Cytokine最新文献

{"title":"Exploring the causal relationship between inflammatory cytokines and myasthenia gravis: A two-way Mendelian randomization study","authors":"Jing-Yu Li ,&nbsp;Yan-Jun Ling ,&nbsp;Wen-Hui Bao ,&nbsp;Wen-Na Zhang ,&nbsp;Xin-Miao Han ,&nbsp;Xiao-Chen Zheng ,&nbsp;Qi Zhao","doi":"10.1016/j.cyto.2024.156843","DOIUrl":"10.1016/j.cyto.2024.156843","url":null,"abstract":"<div><h3>Background</h3><div>Based on previous research, it is well-established that myasthenia gravis (MG) is linked to chronic inflammation. However, the exact nature of the relationship between inflammatory factors and the development of MG remains unclear. Consequently, the objective of this study is to explore whether alterations in the levels of inflammatory factors, as influenced by genetic factors, are associated with the occurrence of MG. This will be achieved through a two-sample Mendelian randomization (MR) analysis.</div></div><div><h3>Methods</h3><div>We conducted a bidirectional Mendelian randomization (MR) study utilizing genetic data from genome-wide association studies (GWAS), encompassing 1873 MG cases and 36,370 individuals of European ancestry as controls. Data on inflammatory cytokines were obtained from GWAS data of 8293, healthy participants. The inverse variance-weighted (IVW) method was primarily employed to investigate the causal relationship between exposure and outcome. Additionally, various sensitivity analysis methods such as MR-Egger, weighted median, simple mode, weighted mode, and MR-PRESSO were applied to strengthen the reliability of the results. Through these rigorous approaches, we extensively examined the relationship between inflammatory factors and MG; however, further research is required to establish the specific causal relationship.</div></div><div><h3>Results</h3><div>After applying Bonferroni correction, the genetic predictions revealed a significant correlation between Monokine induced by gamma interferon (MIG) and MG (OR: 1.09, 95 % CI: 1.04–1.14; <em>P</em> = 0.0006). Furthermore, there were preliminary findings indicating a positive genetic association between Eotaxin and interleukin-2 receptor antagonist (IL-2ra) with MG (OR: 0.81, 95 % CI: 0.66–0.99, <em>P</em> = 0.044; OR: 0.80, 95 % CI: 0.68–0.94, <em>P</em> = 0.008). Reverse MR analysis provided initial evidence of associations between MIP1α, GROa, IL-13, TRAIL, IL-2ra, and IL-1ra with the development of MG. No indications of pleiotropy or heterogeneity among genetic variants were observed (<em>P</em> &gt; 0.05).</div></div><div><h3>Conclusion</h3><div>This study uncovers a new connection between inflammatory cytokines and MG, shedding light on potential factors contributing to the development of the disease. Elevated levels of Eotaxin and IL-2ra are associated with a higher risk of MG, while indicating that MIG, MIP1α, GROa, IL-13, TRAIL, IL-2ra, and IL-1ra may be elevated as a result of MG, Especially MIG. These findings suggest that targeting and regulating specific inflammatory factors could offer promising avenues for the treatment and prevention of MG.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156843"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142908911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interleukin 29 is a novel antiangiogenic factor in angiogenesis","authors":"Man Tu ,&nbsp;Huiping Xu ,&nbsp;Zhengyue Miao ,&nbsp;Yue Wang ,&nbsp;Xiaoke Feng ,&nbsp;Liqun Xie ,&nbsp;Fang Wang","doi":"10.1016/j.cyto.2024.156850","DOIUrl":"10.1016/j.cyto.2024.156850","url":null,"abstract":"<div><h3>Aims</h3><div>Angiogenesis is tightly controlled by growth factors and cytokines in pathophysiological settings. Despite the importance of Interleukin 29 (IL-29), a newly identified cytokine of type III interferon family, its role in angiogenesis remains unknown. We aimed to elucidate IL-29's impact on angiogenesis under both and physiological and pathological conditions.</div></div><div><h3>Methods</h3><div>We employed various assays to evaluate IL-29's effect on proliferation, apoptosis, migration and tube formation of human umbilical vein endothelial cells (HUVEC) in vitro. IL-29's angiogenic effect was assessed using mouse aortic rings ex vivo, and oxygen-induced retinopathy (OIR) mouse model in vivo. Signaling pathways possibly involved in IL-29-induced angiogenesis were investigated by Western blot. Finally, IL-29's impact on tube formation was blocked by inhibiting IL-29/interleukin 10 receptor 2 (IL-10R2) binding.</div></div><div><h3>Results</h3><div>IL-29 treatment inhibited endothelial cell migration, tube formation and vessel sprouting, without affecting proliferation or apoptosis. Notably, IL-29 (100 ng/ml) attenuated vessel growth in pathological angiogenesis in OIR mice, accompanied by decreased expression of vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1α (HIF-1α). Mechanistically, IL-29 activated Stat3 signaling pathway, and blocking IL-29/IL-10R2 binding remarkably reversed IL-29's anti-angiogenic effect on tube formation.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrated that IL-29, at a relative low concentration, modulates angiogenesis in both physiological and pathological contexts. Targeting IL-29 or its receptor IL-10R2 offers a promising strategy for angiogenesis regulation in various conditions.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156850"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When recombinant proteins go wrong: The hidden pitfall of recombinant protein contamination","authors":"Lejla Svraka,&nbsp;Hakim Ben Abdallah,&nbsp;Claus Johansen","doi":"10.1016/j.cyto.2024.156830","DOIUrl":"10.1016/j.cyto.2024.156830","url":null,"abstract":"<div><div>Recombinant proteins are critical tools in research; however, their purity is often assumed rather than verified, leading to potential experimental errors. This study aimed to investigate the inflammatory role of recombinant human IL-17F in dermal fibroblasts. Unexpectedly, we discovered with Western blot that recombinant IL-17F from the supplier was contaminated with IL-4, leading to unintended stimulatory effects such as STAT6 phosphorylation and gene induction of <em>CCL26</em> and <em>IL4R</em>. This contamination led to misinterpretation of data, loss of research time, and erroneous conclusions about IL-17F activity. These findings underscore the critical need for stringent quality control in recombinant protein production and highlight the risks of relying on single-source suppliers. Researchers should remain cautious about potential contamination, ideally validating proteins from multiple suppliers. Our experience illustrates a broader requirement for suppliers to strengthen quality assurance measures, as contaminants can propagate misleading data in the literature and undermine research reproducibility.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156830"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142826895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation of IL-10 and IL18 with the development of liver cirrhosis associated with hepatitis B virus infection: A systematic review","authors":"Mohammad Heiat ,&nbsp;Mohammad Javanbakht ,&nbsp;Davood Jafari ,&nbsp;Mohadeseh Poudineh ,&nbsp;Fatemeh Heydari ,&nbsp;Heidar Sharafi ,&nbsp;Seyed Moayed Alavian","doi":"10.1016/j.cyto.2024.156818","DOIUrl":"10.1016/j.cyto.2024.156818","url":null,"abstract":"<div><h3>Background</h3><div>Patients who have been infected with the Hepatitis B virus (HBV) are susceptible to developing liver cirrhosis (LC) and hepatocellular carcinoma (HCC). The objective of this systematic review was to comprehensively scrutinize the existing evidence concerning the association between host genetic polymorphisms and HBV-associated LC.</div></div><div><h3>Methods</h3><div>We searched databases of PubMed, Scopus, and Web of Science for relevant articles published from building databases to 25 October 2023.</div></div><div><h3>Result</h3><div>We detected 104 relevant articles, relating to 84 individuals genes. Nine genes had the strong evidence of correlation, including IL-10, IL-18, IL-1B, TGF- β, TLR3, STAT4, IL-1RN, Tim3, and IFN receptors. A positive correlation was found for 33 genes but this data had not yet been replicated, 11 genes had limited or mixed evidence of a correlation, and 34 genes indicated no correlation. IL-10 and IL-18 had the most evidence of correlation. There was a notable amount of diversity in both the design and method of studies and data quality.</div></div><div><h3>Conclusion</h3><div>IL-10 and IL-18 had the most evidence of correlation. There was a notable amount of diversity in both the design and method of studies and data quality. It is of necessary to take into account the fundamental mechanism behind these associations and discern those that are confounded by the coexistence of other LC/HCC risk factors and response to therapy. These results are expected to guide future studies on the genetic susceptibility of HBV-related LC/HCC.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156818"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Akkermansia muciniphila activates natural killer cells by suppressing the TGF-β signaling pathway in lung adenocarcinoma cells","authors":"Yong Li ,&nbsp;Huiqin Huang ,&nbsp;Hang Xie ,&nbsp;Rongxiang Cao ,&nbsp;Xiuling Li ,&nbsp;Feijian Huang ,&nbsp;Lu Lin ,&nbsp;Limin Chen","doi":"10.1016/j.cyto.2024.156833","DOIUrl":"10.1016/j.cyto.2024.156833","url":null,"abstract":"<div><div>Lung adenocarcinoma (LUAD) stands out as a prevalent malignant tumor necessitating innovative strategies to enhance therapeutic outcomes. <em>Akkermansia muciniphila</em> (AKK) has emerged as intricately linked to tumor immunotherapy, yet its impact on natural killer (NK) cells, which play a crucial role in immunotherapy, remains unclear. This study aims to investigate the effects of AKK outer membrane proteins on NK cells in LUAD and elucidate potential associated molecular mechanisms. 16S rRNA sequencing was employed to analyze bacterial genera and their abundance in fecal samples from LUAD patients. Co-culturing of NK-92 cells with LUAD cells, with or without treatment of AKK outer membrane protein Amuc_1100, was conducted to investigate the mechanisms of AKK on LUAD. Additionally, a xenograft mouse model was established to validate the effects of AKK in an <em>in vivo</em> setting. The experimental findings indicated that LUAD patients with elevated AKK levels in their fecal samples demonstrated increased NK cell infiltration and reduced TGF-β levels. Treatment with Amuc_1100 elevated TNF-α and IL-15 cytokine levels, decreased TGF-β levels and proteins associated with TGF-β pathway, enhanced NK cell cytotoxicity, upregulated perforin and granzyme B expression, induced apoptosis and cell cycle arrest, thereby inhibiting cancer cell proliferation. Amuc_1100 also impeded tumor growth <em>in vivo</em>. In summary, these results suggest that AKK activates NK cells to target tumor cells by suppressing the TGF-β signaling pathway in LUAD cells, underscoring the potential of Akk as an effective immunotherapeutic agent in LUAD NK cell-directed therapies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156833"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective effect of the vagus nerve-α7nAChR-IL-22 pathway on acute liver injury","authors":"Zhihao Song ,&nbsp;Jing Wu ,&nbsp;Tiemin Jiang ,&nbsp;Rongdong He ,&nbsp;Hao Wen","doi":"10.1016/j.cyto.2024.156840","DOIUrl":"10.1016/j.cyto.2024.156840","url":null,"abstract":"<div><h3>Background</h3><div>Acute liver injury is a common pathological feature of various clinical diseases, and prolonged liver damage can lead to fibrosis and even liver failure. Studies have reported that the vagus nerve can repair liver injury through the regulation of the cholinergic anti-inflammatory pathway. However, there is limited research on the regulation of interleukin-22 and its role in liver injury. This study aimed to investigate the regulatory effect of vagus nerve receptor α7nAChR on interleukin-22 and whether this regulatory axis can protect against liver injury.</div></div><div><h3>Methods</h3><div>Rats and the human liver cell line L-02 were treated with carbon tetrachloride to simulate acute liver injury. The experimental groups were divided as follows: control group, model group, model + PNU282987 group, model + MLA group, and MLA group. After the intervention, blood samples, liver tissues, and cells were collected to assess liver function (AST, ALT), inflammation (TNF-α, IL-6,), α7nAChR and interleukin-22 concentrations, apoptosis levels (Bax, BCL-2), and proliferation markers (Ki-67, PCNA) using quantitative real time PCR, Western blot, immunohistochemistry and ELISA.</div></div><div><h3>Results</h3><div>The results indicated that carbon tetrachloride intervention led to compensatory increases in interleukin-22 while inhibition of α7nAChR decreased interleukin-22 concentrations and exacerbated the injury marked by high levels of AST, ALT and TNF-α,IL-6. Exogenous administration of a vagus nerve agonist alleviated liver injury and was accompanied by an increase in interleukin-22 levels. In rescue experiments, simultaneous inhibition of vagus nerve receptors and administration of exogenous interleukin-22 reduced liver injury and significantly enhanced liver regeneration. Conversely, activation of vagus nerve receptors while inhibiting interleukin-22 aggravated liver injury.</div></div><div><h3>Conclusion</h3><div>This study confirms that vagus nerve receptor α7nAChR can promote liver regeneration and protect against carbon tetrachloride-induced liver injury by regulating interleukin-22.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156840"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142870774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenous binding immunoglobulin protein (BiP) enhance immune regulatory phenotype in ex-vivo Mtb infected PBMCs stratified based on QuantiFERON response","authors":"Bongani Motaung ,&nbsp;Candice Snyders ,&nbsp;Stephanus Malherbe ,&nbsp;Andrea Gutschmidt ,&nbsp;Ilana van Rensburg ,&nbsp;Andre G. Loxton","doi":"10.1016/j.cyto.2024.156832","DOIUrl":"10.1016/j.cyto.2024.156832","url":null,"abstract":"<div><div>Even though anti-tuberculosis (TB) treatment is readily available, <em>Mycobacterium tuberculosis</em> (<em>Mtb</em>) infection continues to be a global threat with a high death rate recorded from a single infectious agent. This highlights the significance of developing new strategies to curb the growing <em>Mtb</em> infection cases. Host-directed therapies (HDT) offer a promising approach that includes both drug discovery and drug repurposing, aimed at identifying host targets and promoting immune cell populations that can lead to better infection outcomes. In this context, we investigated the potential of exogenous Binding Immunoglobulin Protein (BiP) to induce such changes <em>ex-vivo</em> using PBMCs from healthy (QFN-) and <em>Mtb</em> exposed (QFN+) individuals. We analysed cell surface expression and cytokine profiles across eight different stimulation conditions including human full-length BiP protein (20 μg/ml), TLR-9a (0.5 μM), BiP/TLR-9a combination, isoniazid (1 μM), H37Rv (MOI: 1: 10), and pooled bronchoalveolar lavage (BAL) samples collected at TB diagnosis (TBdx) and at month 6 (M6) of anti-TB treatment. Our results revealed that BiP-stimulated PBMCs showed a significant reduction of interleukin (IL)-10 secretion, along with increased IL-4, IL-5, IL-13, and soluble Fas-L (sFasL) secretion. We also observed that BiP stimulation enhanced the expression of membrane bound Fas-L (CD178) and IL5Ra (CD125) in B-cells isolated from both QFN- and QFN+ groups. Additionally, BiP exhibited a synergistic effect with TLR-9a, further boosting this co-expression. Moreover, we observed that BiP induced IL5Ra expression in both CD3⁺CD5^lo and CD3⁺CD5^hi T-cell populations. This study explores the effects of exogenous BiP on cell functionality and provides valuable insights into its potential to modulate host cell responses, which could be explored as a host-directed therapy for TB in the future.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156832"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review on critical factor in monocyte adhesion: Nutrients","authors":"Gülsüm Deveci ,&nbsp;Nilüfer Acar Tek","doi":"10.1016/j.cyto.2024.156845","DOIUrl":"10.1016/j.cyto.2024.156845","url":null,"abstract":"<div><div>Endogenous and exogenous factors play a role in endothelial dysfunction. Inflammation, leukocyte adhesion-aggregation, abnormal vascular proliferation, atherosclerosis, and hypertension are among the endogenous factors. Another factor that affects endothelial dysfunction is exogenous factors such as drug treatments, smoking, alcohol, and nutrition. According various studies on nutrition and endothelial function, it is supported that fatty acids, proteins, and phenolic compounds modulate this function. <em>In vitro</em> studies show that nutrients change the adhesion of monocytes to the endothelium. The pathways that play a role in the adhesion process of monocytes are also affected by nutrients. Particularly among these pathways, mTORC1, S6 plaques, monocyte chemotaxis protein, monocyte integrins, monocyte cytokines are transferred to the lesional area selectin protein. In this article, the effects of various nutrients on monocyte adhesion are examined. It explains the changes and possible mechanisms of nutrients such as fatty acids, protein, phenolic compounds, and other dietary components on monocyte adhesion, and examines the relationship between nutrients and monocyte adhesion in our country and allows us to look at our profession from a different perspective. Although not all nutritional elements are included, it is thought that our profession will play a role in taking the first step towards cell studies.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156845"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the mechanism and crosstalk between IL-6 and IL- 1β on M2 macrophages under metabolic stress conditions","authors":"Shawna Yadav,&nbsp;Anusha Prasannan,&nbsp;Kaliyamurthi Venkatachalam,&nbsp;Ambika Binesh","doi":"10.1016/j.cyto.2024.156852","DOIUrl":"10.1016/j.cyto.2024.156852","url":null,"abstract":"<div><div>Macrophages are highly variable immune cells that are important in controlling inflammation and maintaining tissue balance. The ability to polarize into two major types—M1, promoting inflammation, and M2, resolving inflammation and contributing to tissue repair—determines their specific roles in health and disease. M2 macrophages are particularly important for reducing inflammation and promoting tissue regeneration, but their function is shaped mainly by surrounding cells. This is evident in obesity, diabetes, and chronic inflammation. Although many cytokines regulate macrophage polarization, interleukin-6 (IL-6) and interleukin-1β (IL-1β) are major players, but their effects on M2 macrophage behavior under metabolic stress remain unclear. This study describes the intricacies within M2 macrophages concerning IL-6 and IL-1β signaling when under metabolic stress. Though, more frequently than not, IL-6 is labelled as pro-inflammatory, it can also behave as an anti-inflammatory mediator. On the other hand, IL-1β is the main pro-inflammatory agent, particularly in metabolic disorders. The relationship between these cytokines and the macrophages is mediated through important pathways such as JAK/STAT and NFκB, which get perturbed by metabolic stress. Therefore, metabolic stress also alters the functional parameters of macrophages, including alterations in mitochondrial metabolism, glycolytic and oxidative metabolism. Phosphorylation alters the kinetics involved in energy consumption and affects their polarization and their function. However, it has been suggested that IL-6 and IL-1β may work in concert or competition when inducing M2 polarization and, importantly, implicate cytokine release, phagocytic activity, and tissue repair processes. In this review, we discuss the recent literature on the participation of IL-6 and IL-1β cytokines in macrophage polarization and how metabolic stress changes cytokine functions and synergistic relations. A better understanding of these cytokines would serve as an important step toward exploring alternative antiviral strategies directed against metabolic disturbance and, hence, approve further endeavors.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"186 ","pages":"Article 156852"},"PeriodicalIF":3.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ficolin A and ficolin B aggravate poly(I:C) secondary LPS stimulation-induced acute lung injury by modulating alveolar and interstitial macrophages","authors":"Ziqi Hu ,&nbsp;Xu Wu ,&nbsp;Duoduo Yao ,&nbsp;Jianhua Liu ,&nbsp;Qingli Kong ,&nbsp;Yu-Jie Zhou ,&nbsp;Xulong Zhang","doi":"10.1016/j.cyto.2025.156868","DOIUrl":"10.1016/j.cyto.2025.156868","url":null,"abstract":"<div><div>Respiratory viral infection, represented by influenza virus, is easily followed by bacterial infection, the main cause of death. Clinical studies have shown that even mild influenza virus infection followed by secondary bacterial infection can mediate severe pneumonia and lung injury. In this study, mice were intranasally stimulated by polyinosinic-polycytidylic acid [poly(I:C)] followed by lipopolysaccharide (LPS) to simulate respiratory RNA virus secondary Gram-negative bacterial infection. The results demonstrated that poly(I:C) followed by LPS stimulation induced more weight loss, worse lung pathological injury, additional recruitment of neutrophils and interstitial macrophages, and elevated expression of ficolin A/B in the lung neutrophils, alveolar and interstitial macrophages. Knockout of ficolin A/B alleviated the body weight loss, the lung pathological injury, and the pulmonary inflammatory score. Mechanically, knockout of ficolin A/B was associated with reduced interstitial macrophage recruitment and alveolar macrophage exhaustion. These results suggest that ficolin A/B is a potential therapeutic target for severe pneumonia induced by respiratory RNA virus secondary Gram-negative bacterial infection.</div></div>","PeriodicalId":297,"journal":{"name":"Cytokine","volume":"188 ","pages":"Article 156868"},"PeriodicalIF":3.7,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}