Pub Date : 2024-01-20DOI: 10.1186/s12979-023-00405-0
Andrea Aprilia, Kusworini Handono, Hidayat Sujuti, Akhmad Sabarudin, Nuning Winaris
Background: Inflammaging, the characteristics of immunosenescence, characterized by continuous chronic inflammation that could not be resolved. It is not only affect older people but can also occur in young individuals, especially those suffering from chronic inflammatory conditions such as autoimmune disease, malignancy, or chronic infection. This condition led to altered immune function and as consequent immune function is reduced. Detection of immunosenescence has been done by examining the immune risk profile (IRP), which uses flow cytometry. These tests are not always available in health facilities, especially in developing countries and require fresh whole blood samples. Therefore, it is necessary to find biomarkers that can be tested using stored serum to make it easier to refer to the examination. Here we proposed an insight for soluble biomarkers which represented immune cells activities and exhaustion, namely sCD163, sCD28, sCD80, and sCTLA-4. Those markers were reported to be elevated in chronic diseases that caused early aging and easily detected from serum samples using ELISA method, unlike IRP. Therefore, we conclude these soluble markers are beneficial to predict pathological condition of immunosenescence.
Aim: To identify soluble biomarkers that could replace IRP for detecting immunosenescence.
Conclusion: Soluble costimulatory molecule suchsCD163, sCD28, sCD80, and sCTLA-4 are potential biomarkers for detecting immunosenescence.
{"title":"sCD163, sCD28, sCD80, and sCTLA-4 as soluble marker candidates for detecting immunosenescence.","authors":"Andrea Aprilia, Kusworini Handono, Hidayat Sujuti, Akhmad Sabarudin, Nuning Winaris","doi":"10.1186/s12979-023-00405-0","DOIUrl":"10.1186/s12979-023-00405-0","url":null,"abstract":"<p><strong>Background: </strong>Inflammaging, the characteristics of immunosenescence, characterized by continuous chronic inflammation that could not be resolved. It is not only affect older people but can also occur in young individuals, especially those suffering from chronic inflammatory conditions such as autoimmune disease, malignancy, or chronic infection. This condition led to altered immune function and as consequent immune function is reduced. Detection of immunosenescence has been done by examining the immune risk profile (IRP), which uses flow cytometry. These tests are not always available in health facilities, especially in developing countries and require fresh whole blood samples. Therefore, it is necessary to find biomarkers that can be tested using stored serum to make it easier to refer to the examination. Here we proposed an insight for soluble biomarkers which represented immune cells activities and exhaustion, namely sCD163, sCD28, sCD80, and sCTLA-4. Those markers were reported to be elevated in chronic diseases that caused early aging and easily detected from serum samples using ELISA method, unlike IRP. Therefore, we conclude these soluble markers are beneficial to predict pathological condition of immunosenescence.</p><p><strong>Aim: </strong>To identify soluble biomarkers that could replace IRP for detecting immunosenescence.</p><p><strong>Conclusion: </strong>Soluble costimulatory molecule suchsCD163, sCD28, sCD80, and sCTLA-4 are potential biomarkers for detecting immunosenescence.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"21 1","pages":"9"},"PeriodicalIF":7.9,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10799430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139503202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-16DOI: 10.1186/s12979-023-00407-y
Meng He, Jürgen Borlak
<p><b>Correction: Immun Ageing 20, 58 (2023)</b></p><p><b>https://doi.org/10.1186/s12979-023-00373-5</b></p><p>Following publication of the original article [1], the authors reported an error in the HTML version of this article. The graphical abstract displayed is not the correct image but, a copy of Fig. 10 and in addition Fig. 11 is not fully displayed.</p><p>The publishers apologise for this error.</p><p>The original article [1] has been updated.</p><ol data-track-component="outbound reference"><li data-counter="1."><p>He M, Borlak J. A genomic perspective of the aging human and mouse lung with a focus on immune response and cellular senescence. Immun Ageing. 2023;20:58. https://doi.org/10.1186/s12979-023-00373-5.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Centre for Pharmacology and Toxicology, Hannover Medical School, Carl‑Neuberg‑Str. 1, 30625, Hannover, Germany</p><p>Meng He & Jürgen Borlak</p></li></ol><span>Authors</span><ol><li><span>Meng He</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Jürgen Borlak</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li></ol><h3>Corresponding author</h3><p>Correspondence to Jürgen Borlak.</p><h3>Publisher’s Note</h3><p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p><p>The online version of the original article can be found at https://doi.org/10.1186/s12979-023-00373-5.</p><p><b>Open Access</b> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.</p> <p>Reprints and permissions</p><img alt="Check for updates. Verify cu
更正：Immun Ageing 20, 58 (2023)https://doi.org/10.1186/s12979-023-00373-5Following 原文[1]发表后，作者报告了本文 HTML 版本中的一处错误。He M, Borlak J. A genomic perspective of the aging human and mouse lung with a focus on immune response and cellular senescence. Immun Ageing.Immun Ageing.2023;20:58. https://doi.org/10.1186/s12979-023-00373-5.Article CAS PubMed PubMed Central Google Scholar 下载参考文献作者和单位汉诺威医学院药理学和毒理学中心，Carl-Neuberg-Str.1, 30625, Hannover, GermanyMeng He & Jürgen Borlak作者Meng He查看作者发表的文章您也可以在PubMed Google Scholar中搜索该作者Jürgen Borlak查看作者发表的文章您也可以在PubMed Google Scholar中搜索该作者通讯作者致Jürgen Borlak.Publisher's NoteSpringer Nature对出版地图和机构隶属关系中的管辖权主张保持中立。本文采用知识共享署名 4.0 国际许可协议（Creative Commons Attribution 4.0 International License）进行许可，允许以任何媒介或格式使用、共享、改编、分发和复制，但需注明原作者和来源，提供知识共享许可协议的链接，并说明是否进行了修改。本文中的图片或其他第三方材料均包含在文章的知识共享许可协议中，除非在材料的署名栏中另有说明。如果材料未包含在文章的知识共享许可协议中，且您打算使用的材料不符合法律规定或超出许可使用范围，则您需要直接从版权所有者处获得许可。要查看该许可的副本，请访问 http://creativecommons.org/licenses/by/4.0/。除非在数据的信用行中另有说明，否则创作共用公共领域专用免责声明 (http://creativecommons.org/publicdomain/zero/1.0/) 适用于本文提供的数据。转载与许可引用本文He, M., Borlak, J. Correction：以免疫反应和细胞衰老为重点的人肺和小鼠肺衰老的基因组视角。Immun Ageing 21, 8 (2024). https://doi.org/10.1186/s12979-023-00407-yDownload citationPublished: 16 January 2024DOI: https://doi.org/10.1186/s12979-023-00407-yShare this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative.
{"title":"Correction: A genomic perspective of the aging human and mouse lung with a focus on immune response and cellular senescence","authors":"Meng He, Jürgen Borlak","doi":"10.1186/s12979-023-00407-y","DOIUrl":"https://doi.org/10.1186/s12979-023-00407-y","url":null,"abstract":"<p><b>Correction: Immun Ageing 20, 58 (2023)</b></p><p><b>https://doi.org/10.1186/s12979-023-00373-5</b></p><p>Following publication of the original article [1], the authors reported an error in the HTML version of this article. The graphical abstract displayed is not the correct image but, a copy of Fig. 10 and in addition Fig. 11 is not fully displayed.</p><p>The publishers apologise for this error.</p><p>The original article [1] has been updated.</p><ol data-track-component=\"outbound reference\"><li data-counter=\"1.\"><p>He M, Borlak J. A genomic perspective of the aging human and mouse lung with a focus on immune response and cellular senescence. Immun Ageing. 2023;20:58. https://doi.org/10.1186/s12979-023-00373-5.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Centre for Pharmacology and Toxicology, Hannover Medical School, Carl‑Neuberg‑Str. 1, 30625, Hannover, Germany</p><p>Meng He & Jürgen Borlak</p></li></ol><span>Authors</span><ol><li><span>Meng He</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Jürgen Borlak</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li></ol><h3>Corresponding author</h3><p>Correspondence to Jürgen Borlak.</p><h3>Publisher’s Note</h3><p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p><p>The online version of the original article can be found at https://doi.org/10.1186/s12979-023-00373-5.</p><p><b>Open Access</b> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.</p>\u0000<p>Reprints and permissions</p><img alt=\"Check for updates. Verify cu","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"5 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139476885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The Disposable Soma Theory of aging suggests a trade-off between energy allocation for growth, reproduction and somatic maintenance, including immunity. While trade-offs between reproduction and immunity are well documented, those involving growth remain under-explored. Rapid growth might deplete resources, reducing investment in maintenance, potentially leading to earlier or faster senescence and a shorter lifespan. However, rapid growth could limit exposure to parasitism before reaching adulthood, decreasing immunity needs. The insect immunity's components (cellular, enzymatic, and antibacterial) vary in cost, effectiveness, and duration. Despite overall immunity decline (immunosenescence), its components seem to age differently. We hypothesize that investment in these immune components is adjusted based on the resource cost of growth, longevity, and the associated risk of parasitism.
Results: We tested this hypothesis using the mealworm beetle, Tenebrio molitor as our experimental subject. By manipulating the larval environment, including three different temperatures and three relative humidity levels, we achieved a wide range of growth durations and longevities. Our main focus was on the relationship between growth duration, longevity, and specific immune components: hemocyte count, phenoloxidase activity, and antibacterial activity. We measured these immune parameters both before and after exposing the individuals to a standard bacterial immune challenge, enabling us to assess immune responses. These measurements were taken in both young and older adult beetles. Upon altering growth duration and longevity by modifying larval temperature, we observed a more pronounced investment in cellular and antibacterial defenses among individuals with slow growth and extended lifespans. Intriguingly, slower-growing and long-lived beetles exhibited reduced enzymatic activity. Similar results were found when manipulating larval growth duration and adult longevity through variations in relative humidity, with a particular focus on antibacterial activity.
Conclusion: The impact of growth manipulation on immune senescence varies by the specific immune parameter under consideration. Yet, in slow-growing T. molitor, a clear decline in cellular and antibacterial immune responses with age was observed. This decline can be linked to their initially stronger immune response in early life. Furthermore, our study suggests an immune strategy favoring enhanced antibacterial activity among slow-growing and long-lived T. molitor individuals.
{"title":"Growth and longevity modulation through larval environment mediate immunosenescence and immune strategy of Tenebrio molitor.","authors":"Agathe Crosland, Thierry Rigaud, Charlène Develay, Yannick Moret","doi":"10.1186/s12979-023-00409-w","DOIUrl":"10.1186/s12979-023-00409-w","url":null,"abstract":"<p><strong>Background: </strong>The Disposable Soma Theory of aging suggests a trade-off between energy allocation for growth, reproduction and somatic maintenance, including immunity. While trade-offs between reproduction and immunity are well documented, those involving growth remain under-explored. Rapid growth might deplete resources, reducing investment in maintenance, potentially leading to earlier or faster senescence and a shorter lifespan. However, rapid growth could limit exposure to parasitism before reaching adulthood, decreasing immunity needs. The insect immunity's components (cellular, enzymatic, and antibacterial) vary in cost, effectiveness, and duration. Despite overall immunity decline (immunosenescence), its components seem to age differently. We hypothesize that investment in these immune components is adjusted based on the resource cost of growth, longevity, and the associated risk of parasitism.</p><p><strong>Results: </strong>We tested this hypothesis using the mealworm beetle, Tenebrio molitor as our experimental subject. By manipulating the larval environment, including three different temperatures and three relative humidity levels, we achieved a wide range of growth durations and longevities. Our main focus was on the relationship between growth duration, longevity, and specific immune components: hemocyte count, phenoloxidase activity, and antibacterial activity. We measured these immune parameters both before and after exposing the individuals to a standard bacterial immune challenge, enabling us to assess immune responses. These measurements were taken in both young and older adult beetles. Upon altering growth duration and longevity by modifying larval temperature, we observed a more pronounced investment in cellular and antibacterial defenses among individuals with slow growth and extended lifespans. Intriguingly, slower-growing and long-lived beetles exhibited reduced enzymatic activity. Similar results were found when manipulating larval growth duration and adult longevity through variations in relative humidity, with a particular focus on antibacterial activity.</p><p><strong>Conclusion: </strong>The impact of growth manipulation on immune senescence varies by the specific immune parameter under consideration. Yet, in slow-growing T. molitor, a clear decline in cellular and antibacterial immune responses with age was observed. This decline can be linked to their initially stronger immune response in early life. Furthermore, our study suggests an immune strategy favoring enhanced antibacterial activity among slow-growing and long-lived T. molitor individuals.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"21 1","pages":"7"},"PeriodicalIF":7.9,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10785379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139425977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-11DOI: 10.1186/s12979-023-00406-z
Janet M. Lord, Tonny Veenith, Jack Sullivan, Archana Sharma-Oates, Alex G. Richter, Neil J. Greening, Hamish J. C. McAuley, Rachael A. Evans, Paul Moss, Shona C. Moore, Lance Turtle, Nandan Gautam, Ahmed Gilani, Manan Bajaj, Louise V. Wain, Christopher Brightling, Betty Raman, Michael Marks, Amisha Singapuri, Omer Elneima, Peter J. M. Openshaw, Niharika A. Duggal
The striking increase in COVID-19 severity in older adults provides a clear example of immunesenescence, the age-related remodelling of the immune system. To better characterise the association between convalescent immunesenescence and acute disease severity, we determined the immune phenotype of COVID-19 survivors and non-infected controls. We performed detailed immune phenotyping of peripheral blood mononuclear cells isolated from 103 COVID-19 survivors 3–5 months post recovery who were classified as having had severe (n = 56; age 53.12 ± 11.30 years), moderate (n = 32; age 52.28 ± 11.43 years) or mild (n = 15; age 49.67 ± 7.30 years) disease and compared with age and sex-matched healthy adults (n = 59; age 50.49 ± 10.68 years). We assessed a broad range of immune cell phenotypes to generate a composite score, IMM-AGE, to determine the degree of immune senescence. We found increased immunesenescence features in severe COVID-19 survivors compared to controls including: a reduced frequency and number of naïve CD4 and CD8 T cells (p < 0.0001); increased frequency of EMRA CD4 (p < 0.003) and CD8 T cells (p < 0.001); a higher frequency (p < 0.0001) and absolute numbers (p < 0.001) of CD28−ve CD57+ve senescent CD4 and CD8 T cells; higher frequency (p < 0.003) and absolute numbers (p < 0.02) of PD-1 expressing exhausted CD8 T cells; a two-fold increase in Th17 polarisation (p < 0.0001); higher frequency of memory B cells (p < 0.001) and increased frequency (p < 0.0001) and numbers (p < 0.001) of CD57+ve senescent NK cells. As a result, the IMM-AGE score was significantly higher in severe COVID-19 survivors than in controls (p < 0.001). Few differences were seen for those with moderate disease and none for mild disease. Regression analysis revealed the only pre-existing variable influencing the IMM-AGE score was South Asian ethnicity ( $$beta$$ = 0.174, p = 0.043), with a major influence being disease severity ( $$beta$$ = 0.188, p = 0.01). Our analyses reveal a state of enhanced immune ageing in survivors of severe COVID-19 and suggest this could be related to SARS-Cov-2 infection. Our data support the rationale for trials of anti-immune ageing interventions for improving clinical outcomes in these patients with severe disease.
{"title":"Accelarated immune ageing is associated with COVID-19 disease severity","authors":"Janet M. Lord, Tonny Veenith, Jack Sullivan, Archana Sharma-Oates, Alex G. Richter, Neil J. Greening, Hamish J. C. McAuley, Rachael A. Evans, Paul Moss, Shona C. Moore, Lance Turtle, Nandan Gautam, Ahmed Gilani, Manan Bajaj, Louise V. Wain, Christopher Brightling, Betty Raman, Michael Marks, Amisha Singapuri, Omer Elneima, Peter J. M. Openshaw, Niharika A. Duggal","doi":"10.1186/s12979-023-00406-z","DOIUrl":"https://doi.org/10.1186/s12979-023-00406-z","url":null,"abstract":"The striking increase in COVID-19 severity in older adults provides a clear example of immunesenescence, the age-related remodelling of the immune system. To better characterise the association between convalescent immunesenescence and acute disease severity, we determined the immune phenotype of COVID-19 survivors and non-infected controls. We performed detailed immune phenotyping of peripheral blood mononuclear cells isolated from 103 COVID-19 survivors 3–5 months post recovery who were classified as having had severe (n = 56; age 53.12 ± 11.30 years), moderate (n = 32; age 52.28 ± 11.43 years) or mild (n = 15; age 49.67 ± 7.30 years) disease and compared with age and sex-matched healthy adults (n = 59; age 50.49 ± 10.68 years). We assessed a broad range of immune cell phenotypes to generate a composite score, IMM-AGE, to determine the degree of immune senescence. We found increased immunesenescence features in severe COVID-19 survivors compared to controls including: a reduced frequency and number of naïve CD4 and CD8 T cells (p < 0.0001); increased frequency of EMRA CD4 (p < 0.003) and CD8 T cells (p < 0.001); a higher frequency (p < 0.0001) and absolute numbers (p < 0.001) of CD28−ve CD57+ve senescent CD4 and CD8 T cells; higher frequency (p < 0.003) and absolute numbers (p < 0.02) of PD-1 expressing exhausted CD8 T cells; a two-fold increase in Th17 polarisation (p < 0.0001); higher frequency of memory B cells (p < 0.001) and increased frequency (p < 0.0001) and numbers (p < 0.001) of CD57+ve senescent NK cells. As a result, the IMM-AGE score was significantly higher in severe COVID-19 survivors than in controls (p < 0.001). Few differences were seen for those with moderate disease and none for mild disease. Regression analysis revealed the only pre-existing variable influencing the IMM-AGE score was South Asian ethnicity ( $$beta$$ = 0.174, p = 0.043), with a major influence being disease severity ( $$beta$$ = 0.188, p = 0.01). Our analyses reveal a state of enhanced immune ageing in survivors of severe COVID-19 and suggest this could be related to SARS-Cov-2 infection. Our data support the rationale for trials of anti-immune ageing interventions for improving clinical outcomes in these patients with severe disease. ","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"13 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2024-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139422283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-10DOI: 10.1186/s12979-024-00411-w
Moisés E. Bauer, Graham Pawelec, Roberto Paganelli
<p>For decades, the central nervous system (CNS) was known as an immune-privileged site. This concept was formulated based on experimental studies that demonstrated that, unlike what was observed in peripheral organs, skin grafts were not rejected when transplanted into the brain parenchyma. The presence of the blood-brain barrier (BBB), capable of selectively regulating the entry of molecules and cells from the bloodstream into the brain parenchyma, and the absence of conventional lymphatic vessels contributed to reinforcing this concept [1]. However, meningeal lymphatic vessels in the dura mater and, more recently, glymphatic vessels have raised questions about the dogma of the CNS as an immune-privileged site [2, 3]. The CNS has thus adopted mechanisms that enable communication with the immune system, which is crucial for a healthy brain.</p><p>Recent studies highlight the borders of the CNS as pivotal sites of neuro-immune interactions. Under physiological conditions, characterized by the absence of leukocytes in the brain parenchyma, innate immune cells, such as macrophages, and adaptive immune cells, such as T and B cells, are present in meningeal regions, in the choroid plexus and perivascular spaces. In addition to actively participating in immune surveillance in the CNS, these cells contribute to the maintenance of brain homeostasis and may influence behavioural and cognitive responses [4, 5]. For instance, cytokines secreted by immune cells, localized at the brain borders, may change behaviour through modulation of neuronal activities in distinct brain regions [5]. Indeed, several T cell-related cytokines have been shown to modulate complex CNS functions, by inducing changes in neuronal physiology: interferon γ (IFN-γ) alters sociability [6], IL-17 maintains anxiety and spatial learning [7], and IL-4 regulates learning and memory [8].</p><p>Inflammaging is a low level pro-inflammatory state which is believed to be a major contributor to biological aging which underlies many age-associated diseases. Peripheral inflammation significantly affects brain function and contributes to the development of several neurological disorders. Changes in interactions between the CNS and the immune system, such as those observed during ageing, could predispose to the development of neurodegenerative and neuropsychiatric diseases. Both ageing and neuropsychiatric disorders of older adults seem to converge on the pathogenetic role of inflammation, hence the notion of neuroinflammation. Increasing evidence indicates the role of neuroinflammation in age-related neurodegenerative diseases, such as Alzheimer’s Disease (AD) and Parkinson’s disease (PD). The neuropathological features of these diseases include aggregation and accumulation of intracellular and/or extracellular proteins that are associated with neuronal loss in specific regions of the brain. Furthermore, proliferation and activation of glial cells (i.e., “gliosis”) are well established in these di
{"title":"Neuroimmunology and ageing – the state of the art","authors":"Moisés E. Bauer, Graham Pawelec, Roberto Paganelli","doi":"10.1186/s12979-024-00411-w","DOIUrl":"https://doi.org/10.1186/s12979-024-00411-w","url":null,"abstract":"<p>For decades, the central nervous system (CNS) was known as an immune-privileged site. This concept was formulated based on experimental studies that demonstrated that, unlike what was observed in peripheral organs, skin grafts were not rejected when transplanted into the brain parenchyma. The presence of the blood-brain barrier (BBB), capable of selectively regulating the entry of molecules and cells from the bloodstream into the brain parenchyma, and the absence of conventional lymphatic vessels contributed to reinforcing this concept [1]. However, meningeal lymphatic vessels in the dura mater and, more recently, glymphatic vessels have raised questions about the dogma of the CNS as an immune-privileged site [2, 3]. The CNS has thus adopted mechanisms that enable communication with the immune system, which is crucial for a healthy brain.</p><p>Recent studies highlight the borders of the CNS as pivotal sites of neuro-immune interactions. Under physiological conditions, characterized by the absence of leukocytes in the brain parenchyma, innate immune cells, such as macrophages, and adaptive immune cells, such as T and B cells, are present in meningeal regions, in the choroid plexus and perivascular spaces. In addition to actively participating in immune surveillance in the CNS, these cells contribute to the maintenance of brain homeostasis and may influence behavioural and cognitive responses [4, 5]. For instance, cytokines secreted by immune cells, localized at the brain borders, may change behaviour through modulation of neuronal activities in distinct brain regions [5]. Indeed, several T cell-related cytokines have been shown to modulate complex CNS functions, by inducing changes in neuronal physiology: interferon γ (IFN-γ) alters sociability [6], IL-17 maintains anxiety and spatial learning [7], and IL-4 regulates learning and memory [8].</p><p>Inflammaging is a low level pro-inflammatory state which is believed to be a major contributor to biological aging which underlies many age-associated diseases. Peripheral inflammation significantly affects brain function and contributes to the development of several neurological disorders. Changes in interactions between the CNS and the immune system, such as those observed during ageing, could predispose to the development of neurodegenerative and neuropsychiatric diseases. Both ageing and neuropsychiatric disorders of older adults seem to converge on the pathogenetic role of inflammation, hence the notion of neuroinflammation. Increasing evidence indicates the role of neuroinflammation in age-related neurodegenerative diseases, such as Alzheimer’s Disease (AD) and Parkinson’s disease (PD). The neuropathological features of these diseases include aggregation and accumulation of intracellular and/or extracellular proteins that are associated with neuronal loss in specific regions of the brain. Furthermore, proliferation and activation of glial cells (i.e., “gliosis”) are well established in these di","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"17 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139414187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-06DOI: 10.1186/s12979-023-00410-3
Yiming Pan, Lina Ma
Global population aging poses a tremendous burden on the health care system worldwide. Frailty is associated with decreased physical reserve and is considered an important indicator of adverse events in the older population. Therefore, there is growing interest in the early diagnosis and intervention of frailty, but the cellular mechanisms responsible for frailty are still not completely understood. Chronic inflammation is related to decreased physical function and increased disease risk. Additionally, multiple human and animal studies suggest that inflammation probably plays the largest role in contributing to frailty. Some inflammatory markers have been proposed to predict physical frailty. However, there are still large gaps in knowledge related to the clinical application of these markers in frail patients. Therefore, understanding the biological processes and identifying recognized and reliable markers are urgent and pivotal tasks for geriatricians. In the present review, we broadly summarize the inflammatory markers that may have potential diagnostic and therapeutic use, thereby translating them into health care for older people with frailty in the near future.
{"title":"Inflammatory markers and physical frailty: towards clinical application.","authors":"Yiming Pan, Lina Ma","doi":"10.1186/s12979-023-00410-3","DOIUrl":"10.1186/s12979-023-00410-3","url":null,"abstract":"<p><p>Global population aging poses a tremendous burden on the health care system worldwide. Frailty is associated with decreased physical reserve and is considered an important indicator of adverse events in the older population. Therefore, there is growing interest in the early diagnosis and intervention of frailty, but the cellular mechanisms responsible for frailty are still not completely understood. Chronic inflammation is related to decreased physical function and increased disease risk. Additionally, multiple human and animal studies suggest that inflammation probably plays the largest role in contributing to frailty. Some inflammatory markers have been proposed to predict physical frailty. However, there are still large gaps in knowledge related to the clinical application of these markers in frail patients. Therefore, understanding the biological processes and identifying recognized and reliable markers are urgent and pivotal tasks for geriatricians. In the present review, we broadly summarize the inflammatory markers that may have potential diagnostic and therapeutic use, thereby translating them into health care for older people with frailty in the near future.</p>","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"21 1","pages":"4"},"PeriodicalIF":7.9,"publicationDate":"2024-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10770917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139111343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-02DOI: 10.1186/s12979-023-00404-1
Bang-rong Wei, Yu-jia Zhao, Yu-feng Cheng, Chun Huang, Feng Zhang
Parkinson’s disease (PD), a neurodegenerative disorder with an unknown etiology, is primarily characterized by the degeneration of dopamine (DA) neurons. The prevalence of PD has experienced a significant surge in recent years. The unidentified etiology poses limitations to the development of effective therapeutic interventions for this condition. Helicobacter pylori (H. pylori) infection has affected approximately half of the global population. Mounting evidences suggest that H. pylori infection plays an important role in PD through various mechanisms. The autotoxin produced by H. pylori induces pro-inflammatory cytokines release, thereby facilitating the occurrence of central inflammation that leads to neuronal damage. Simultaneously, H. pylori disrupts the equilibrium of gastrointestinal microbiota with an overgrowth of bacteria in the small intestinal known as small intestinal bacterial overgrowth (SIBO). This dysbiosis of the gut flora influences the central nervous system (CNS) through microbiome-gut-brain axis. Moreover, SIBO hampers levodopa absorption and affects its therapeutic efficacy in the treatment of PD. Also, H. pylori promotes the production of defensins to regulate the permeability of the blood-brain barrier, facilitating the entry of harmful factors into the CNS. In addition, H. pylori has been found to induce gastroparesis, resulting in a prolonged transit time for levodopa to reach the small intestine. H. pylori may exploit levodopa to facilitate its own growth and proliferation, or it can inflict damage to the gastrointestinal mucosa, leading to gastrointestinal ulcers and impeding levodopa absorption. Here, this review focused on the role of H. pylori infection in PD from etiology, pathogenesis to levodopa bioavailability.
{"title":"Helicobacter pylori infection and Parkinson’s Disease: etiology, pathogenesis and levodopa bioavailability","authors":"Bang-rong Wei, Yu-jia Zhao, Yu-feng Cheng, Chun Huang, Feng Zhang","doi":"10.1186/s12979-023-00404-1","DOIUrl":"https://doi.org/10.1186/s12979-023-00404-1","url":null,"abstract":"Parkinson’s disease (PD), a neurodegenerative disorder with an unknown etiology, is primarily characterized by the degeneration of dopamine (DA) neurons. The prevalence of PD has experienced a significant surge in recent years. The unidentified etiology poses limitations to the development of effective therapeutic interventions for this condition. Helicobacter pylori (H. pylori) infection has affected approximately half of the global population. Mounting evidences suggest that H. pylori infection plays an important role in PD through various mechanisms. The autotoxin produced by H. pylori induces pro-inflammatory cytokines release, thereby facilitating the occurrence of central inflammation that leads to neuronal damage. Simultaneously, H. pylori disrupts the equilibrium of gastrointestinal microbiota with an overgrowth of bacteria in the small intestinal known as small intestinal bacterial overgrowth (SIBO). This dysbiosis of the gut flora influences the central nervous system (CNS) through microbiome-gut-brain axis. Moreover, SIBO hampers levodopa absorption and affects its therapeutic efficacy in the treatment of PD. Also, H. pylori promotes the production of defensins to regulate the permeability of the blood-brain barrier, facilitating the entry of harmful factors into the CNS. In addition, H. pylori has been found to induce gastroparesis, resulting in a prolonged transit time for levodopa to reach the small intestine. H. pylori may exploit levodopa to facilitate its own growth and proliferation, or it can inflict damage to the gastrointestinal mucosa, leading to gastrointestinal ulcers and impeding levodopa absorption. Here, this review focused on the role of H. pylori infection in PD from etiology, pathogenesis to levodopa bioavailability.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"39 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139078395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-02DOI: 10.1186/s12979-023-00402-3
Cristina Rodriguez-Rodriguez, Natalia González-Mancha, Ane Ochoa-Echeverría, Rosa Liébana, Isabel Merida
Sorting Nexin 27 (SNX27)-retromer complex facilitates cargo recycling from endosomes to the plasma membrane. SNX27 downregulation in neurons, as the result of Trisomy 21 (T21), has been linked with cognitive deficits due to impairment of AMPA and NMDA receptor recycling. Studies in human T cell lines likewise demonstrated that SNX27 regulates the correct delivery of cargoes to the immune synapse limiting the activation of pro-inflammatory pathways. Nevertheless, the physiological consequences of partial SNX27 loss in T cell homeostasis are still unclear. In this study, we have explored the consequences of T cell specific partial SNX27 downregulation in mice. T cells with partial SNX27 deficiency show a marked deficit in the CD4+ T cell pool, a hallmark of aging in mice and humans, and a well-characterized comorbidity of individuals with Down syndrome (DS). When analyzed ex vivo, CD4+ T cells with partial SNX27 deletion demonstrate enhanced proliferation but diminished IL-2 production. In contrast, the CD8+ population show enhanced expression of pro-inflammatory cytokines and lytic enzymes. This mouse model supports the relevance of SNX27 in the organization of the immune synapse, previously described in cell lines, as well as in the control of T cell homeostasis. Individuals with DS experiment an acceleration of the aging process, which particularly affects the immune and central nervous systems. Thus, we hypothesize that reduced SNX27 expression in DS could contribute to the dysregulation of these systems and further research in SNX27 will shed light on the molecular factors underlying the phenotypes observed in people with DS and its contribution to aging.
分选内含蛋白 27（SNX27）-转录因子复合物促进了货物从内体到质膜的再循环。由于 21 三体综合征（T21），神经元中的 SNX27 下调与 AMPA 和 NMDA 受体循环受损导致的认知障碍有关。在人类 T 细胞系中进行的研究同样表明，SNX27 可调节货物向免疫突触的正确传递，从而限制促炎途径的激活。然而，部分 SNX27 缺失对 T 细胞稳态的生理影响仍不清楚。在这项研究中，我们探讨了小鼠T细胞特异性SNX27部分下调的后果。部分 SNX27 缺失的 T 细胞在 CD4+ T 细胞池中显示出明显的缺陷，这是小鼠和人类衰老的标志，也是唐氏综合征（DS）患者的一种特征明显的合并症。在进行体外分析时，部分 SNX27 缺失的 CD4+ T 细胞显示出增殖增强，但 IL-2 生成减少。与此相反，CD8+细胞群的促炎细胞因子和裂解酶表达增强。这一小鼠模型证实了 SNX27 与免疫突触的组织以及 T 细胞稳态控制的相关性。DS 患者的衰老过程会加速，这尤其会影响免疫系统和中枢神经系统。因此，我们推测SNX27在DS患者中的表达减少可能会导致这些系统的失调，对SNX27的进一步研究将揭示在DS患者中观察到的表型的分子因素及其对衰老的贡献。
{"title":"Partial loss of Sorting Nexin 27 resembles age- and Down syndrome-associated T cell dysfunctions","authors":"Cristina Rodriguez-Rodriguez, Natalia González-Mancha, Ane Ochoa-Echeverría, Rosa Liébana, Isabel Merida","doi":"10.1186/s12979-023-00402-3","DOIUrl":"https://doi.org/10.1186/s12979-023-00402-3","url":null,"abstract":"Sorting Nexin 27 (SNX27)-retromer complex facilitates cargo recycling from endosomes to the plasma membrane. SNX27 downregulation in neurons, as the result of Trisomy 21 (T21), has been linked with cognitive deficits due to impairment of AMPA and NMDA receptor recycling. Studies in human T cell lines likewise demonstrated that SNX27 regulates the correct delivery of cargoes to the immune synapse limiting the activation of pro-inflammatory pathways. Nevertheless, the physiological consequences of partial SNX27 loss in T cell homeostasis are still unclear. In this study, we have explored the consequences of T cell specific partial SNX27 downregulation in mice. T cells with partial SNX27 deficiency show a marked deficit in the CD4+ T cell pool, a hallmark of aging in mice and humans, and a well-characterized comorbidity of individuals with Down syndrome (DS). When analyzed ex vivo, CD4+ T cells with partial SNX27 deletion demonstrate enhanced proliferation but diminished IL-2 production. In contrast, the CD8+ population show enhanced expression of pro-inflammatory cytokines and lytic enzymes. This mouse model supports the relevance of SNX27 in the organization of the immune synapse, previously described in cell lines, as well as in the control of T cell homeostasis. Individuals with DS experiment an acceleration of the aging process, which particularly affects the immune and central nervous systems. Thus, we hypothesize that reduced SNX27 expression in DS could contribute to the dysregulation of these systems and further research in SNX27 will shed light on the molecular factors underlying the phenotypes observed in people with DS and its contribution to aging.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"40 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139078394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aging is a holistic change that has a major impact on the immune system, and immunosenescence contributes to the overall progression of aging. The bone marrow is the most important hematopoietic immune organ, while the spleen, as the most important extramedullary hematopoietic immune organ, maintains homeostasis of the human hematopoietic immune system (HIS) in cooperation with the bone marrow. However, the overall changes in the HIS during aging have not been described. Here, we describe a hematopoietic immune map of the spleen and bone marrow of young and old mice using single-cell sequencing and flow cytometry techniques. We observed extensive, complex changes in the HIS during aging. Compared with young mice, the immune cells of aged mice showed a marked tendency toward myeloid differentiation, with the neutrophil population accounting for a significant proportion of this response. In this change, hypoxia-inducible factor 1-alpha (Hif1α) was significantly overexpressed, and this enhanced the immune efficacy and inflammatory response of neutrophils. Our research revealed that during the aging process, hematopoietic stem cells undergo significant changes in function and composition, and their polymorphism and differentiation abilities are downregulated. Moreover, we found that the highly responsive CD62L + HSCs were obviously downregulated in aging, suggesting that they may play an important role in the aging process. Overall, aging extensively alters the cellular composition and function of the HIS. These findings could potentially give high-dimensional insights and enable more accurate functional and developmental analyses as well as immune monitoring in HIS aging.
衰老是一种整体性变化，对免疫系统有重大影响，而免疫衰老则是衰老整体进展的一个重要因素。骨髓是最重要的造血免疫器官，而脾脏作为最重要的髓外造血免疫器官，与骨髓共同维持人体造血免疫系统（HIS）的平衡。然而，造血免疫系统在衰老过程中的整体变化尚未得到描述。在这里，我们利用单细胞测序和流式细胞仪技术描述了年轻和年老小鼠脾脏和骨髓的造血免疫图谱。我们观察到 HIS 在衰老过程中发生了广泛而复杂的变化。与年轻小鼠相比，衰老小鼠的免疫细胞表现出明显的髓系分化趋势，其中中性粒细胞群体在这一反应中占了很大比例。在这一变化中，缺氧诱导因子1-α（Hif1α）明显过度表达，这增强了中性粒细胞的免疫功效和炎症反应。我们的研究发现，在衰老过程中，造血干细胞的功能和组成会发生重大变化，其多态性和分化能力会被下调。此外，我们发现高反应性的 CD62L + 造血干细胞在衰老过程中明显下调，这表明它们可能在衰老过程中扮演重要角色。总之，衰老会广泛改变 HIS 的细胞组成和功能。这些发现有可能提供高维度的见解，并能对 HIS 的衰老过程进行更准确的功能和发育分析以及免疫监测。
{"title":"An aging-related immune landscape in the hematopoietic immune system","authors":"Jianjie Lv, Chun Zhang, Xiuxing Liu, Chenyang Gu, Yidan Liu, Yuehan Gao, Zhaohao Huang, Qi Jiang, Binyao Chen, Daquan He, Tianfu Wang, Zhuping Xu, Wenru Su","doi":"10.1186/s12979-023-00403-2","DOIUrl":"https://doi.org/10.1186/s12979-023-00403-2","url":null,"abstract":"Aging is a holistic change that has a major impact on the immune system, and immunosenescence contributes to the overall progression of aging. The bone marrow is the most important hematopoietic immune organ, while the spleen, as the most important extramedullary hematopoietic immune organ, maintains homeostasis of the human hematopoietic immune system (HIS) in cooperation with the bone marrow. However, the overall changes in the HIS during aging have not been described. Here, we describe a hematopoietic immune map of the spleen and bone marrow of young and old mice using single-cell sequencing and flow cytometry techniques. We observed extensive, complex changes in the HIS during aging. Compared with young mice, the immune cells of aged mice showed a marked tendency toward myeloid differentiation, with the neutrophil population accounting for a significant proportion of this response. In this change, hypoxia-inducible factor 1-alpha (Hif1α) was significantly overexpressed, and this enhanced the immune efficacy and inflammatory response of neutrophils. Our research revealed that during the aging process, hematopoietic stem cells undergo significant changes in function and composition, and their polymorphism and differentiation abilities are downregulated. Moreover, we found that the highly responsive CD62L + HSCs were obviously downregulated in aging, suggesting that they may play an important role in the aging process. Overall, aging extensively alters the cellular composition and function of the HIS. These findings could potentially give high-dimensional insights and enable more accurate functional and developmental analyses as well as immune monitoring in HIS aging.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"26 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139078397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-12-18DOI: 10.1186/s12979-023-00401-4
Robertina Giacconi, Patrizia D’Aquila, Maurizio Cardelli, Francesco Piacenza, Elisa Pierpaoli, Giada Sena, Mirko Di Rosa, Anna Rita Bonfigli, Roberta Galeazzi, Antonio Cherubini, Massimiliano Fedecostante, Riccardo Sarzani, Chiara Di Pentima, Piero Giordano, Roberto Antonicelli, Fabrizia Lattanzio, Giuseppe Passarino, Mauro Provinciali, Dina Bellizzi
Coronavirus disease COVID-19 is a heterogeneous condition caused by SARS-CoV-2 infection. Generally, it is characterized by interstitial pneumonia that can lead to impaired gas-exchange, acute respiratory failure, and death, although a complex disorder of multi-organ dysfunction has also been described. The pathogenesis is complex, and a variable combination of factors has been described in critically ill patients. COVID-19 is a particular risk for older persons, particularly those with frailty and comorbidities. Blood bacterial DNA has been reported in both physiological and pathological conditions and has been associated with some haematological and laboratory parameters but, to date, no study has characterized it in hospitalized old COVID-19 patients The present study aimed to establish an association between blood bacterial DNA (BB-DNA) and clinical severity in old COVID-19 patients. BB-DNA levels were determined, by quantitative real-time PCRs targeting the 16S rRNA gene, in 149 hospitalized older patients (age range 65–99 years) with COVID-19. Clinical data, including symptoms and signs of infection, frailty status, and comorbidities, were assessed. BB-DNA was increased in deceased patients compared to discharged ones, and Cox regression analysis confirmed an association between BB-DNA and in-hospital mortality. Furthermore, BB-DNA was positively associated with the neutrophil count and negatively associated with plasma IFN-alpha. Additionally, BB-DNA was associated with diabetes. The association of BB-DNA with mortality, immune-inflammatory parameters and diabetes in hospitalized COVID-19 patients suggests its potential role as a biomarker of unfavourable outcomes of the disease, thus it could be proposed as a novel prognostic marker in the assessment of acute COVID-19 disease.
{"title":"Blood circulating bacterial DNA in hospitalized old COVID-19 patients","authors":"Robertina Giacconi, Patrizia D’Aquila, Maurizio Cardelli, Francesco Piacenza, Elisa Pierpaoli, Giada Sena, Mirko Di Rosa, Anna Rita Bonfigli, Roberta Galeazzi, Antonio Cherubini, Massimiliano Fedecostante, Riccardo Sarzani, Chiara Di Pentima, Piero Giordano, Roberto Antonicelli, Fabrizia Lattanzio, Giuseppe Passarino, Mauro Provinciali, Dina Bellizzi","doi":"10.1186/s12979-023-00401-4","DOIUrl":"https://doi.org/10.1186/s12979-023-00401-4","url":null,"abstract":"Coronavirus disease COVID-19 is a heterogeneous condition caused by SARS-CoV-2 infection. Generally, it is characterized by interstitial pneumonia that can lead to impaired gas-exchange, acute respiratory failure, and death, although a complex disorder of multi-organ dysfunction has also been described. The pathogenesis is complex, and a variable combination of factors has been described in critically ill patients. COVID-19 is a particular risk for older persons, particularly those with frailty and comorbidities. Blood bacterial DNA has been reported in both physiological and pathological conditions and has been associated with some haematological and laboratory parameters but, to date, no study has characterized it in hospitalized old COVID-19 patients The present study aimed to establish an association between blood bacterial DNA (BB-DNA) and clinical severity in old COVID-19 patients. BB-DNA levels were determined, by quantitative real-time PCRs targeting the 16S rRNA gene, in 149 hospitalized older patients (age range 65–99 years) with COVID-19. Clinical data, including symptoms and signs of infection, frailty status, and comorbidities, were assessed. BB-DNA was increased in deceased patients compared to discharged ones, and Cox regression analysis confirmed an association between BB-DNA and in-hospital mortality. Furthermore, BB-DNA was positively associated with the neutrophil count and negatively associated with plasma IFN-alpha. Additionally, BB-DNA was associated with diabetes. The association of BB-DNA with mortality, immune-inflammatory parameters and diabetes in hospitalized COVID-19 patients suggests its potential role as a biomarker of unfavourable outcomes of the disease, thus it could be proposed as a novel prognostic marker in the assessment of acute COVID-19 disease.","PeriodicalId":51289,"journal":{"name":"Immunity & Ageing","volume":"93 1","pages":""},"PeriodicalIF":7.9,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138716098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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