Pub Date : 2024-01-01Epub Date: 2024-08-21DOI: 10.1159/000540959
Rainer H Straub, Maurizio Cutolo
Background: All active scientists stand on the shoulders of giants and many other more anonymous scientists, and this is not different in our field of psycho-neuro-endocrine immunology in rheumatic diseases. Too often, the modern world of publishing forgets about the collective enterprise of scientists. Some journals advise the authors to present only literature from the last decade, and it has become a natural attitude of many scientists to present only the latest publications. In order to work against this general unempirical behavior, neuroimmunomodulation devotes the 30th anniversary issue to the history of medical science in psycho-neuro-endocrine immunology.
Summary: Keywords were derived from the psycho-neuro-endocrine immunology research field very well known to the authors (R.H.S. has collected a list of keywords since 1994). We screened PubMed, the Cochran Library of Medicine, Embase, Scopus database, and the ORCID database to find relevant historical literature. The Snowballing procedure helped find related work. According to the historical appearance of discoveries in the field, the order of presentation follows the subsequent scheme: (1) the sensory nervous system, (2) the sympathetic nervous system, (3) the vagus nerve, (4) steroid hormones (glucocorticoids, androgens, progesterone, estrogens, and the vitamin D hormone), (5) afferent pathways involved in fatigue, anxiety, insomnia, and depression (includes pathophysiology), and (6) evolutionary medicine and energy regulation - an umbrella theory.
Key messages: A brief history on psycho-neuro-endocrine immunology cannot address all relevant aspects of the field. The authors are aware of this shortcoming. The reader must see this review as a viewpoint through the biased eyes of the authors. Nevertheless, the text gives an overview of the history in psycho-neuro-endocrine immunology of rheumatic diseases.
{"title":"A History of Psycho-Neuro-Endocrine Immune Interactions in Rheumatic Diseases.","authors":"Rainer H Straub, Maurizio Cutolo","doi":"10.1159/000540959","DOIUrl":"10.1159/000540959","url":null,"abstract":"<p><strong>Background: </strong>All active scientists stand on the shoulders of giants and many other more anonymous scientists, and this is not different in our field of psycho-neuro-endocrine immunology in rheumatic diseases. Too often, the modern world of publishing forgets about the collective enterprise of scientists. Some journals advise the authors to present only literature from the last decade, and it has become a natural attitude of many scientists to present only the latest publications. In order to work against this general unempirical behavior, neuroimmunomodulation devotes the 30th anniversary issue to the history of medical science in psycho-neuro-endocrine immunology.</p><p><strong>Summary: </strong>Keywords were derived from the psycho-neuro-endocrine immunology research field very well known to the authors (R.H.S. has collected a list of keywords since 1994). We screened PubMed, the Cochran Library of Medicine, Embase, Scopus database, and the ORCID database to find relevant historical literature. The Snowballing procedure helped find related work. According to the historical appearance of discoveries in the field, the order of presentation follows the subsequent scheme: (1) the sensory nervous system, (2) the sympathetic nervous system, (3) the vagus nerve, (4) steroid hormones (glucocorticoids, androgens, progesterone, estrogens, and the vitamin D hormone), (5) afferent pathways involved in fatigue, anxiety, insomnia, and depression (includes pathophysiology), and (6) evolutionary medicine and energy regulation - an umbrella theory.</p><p><strong>Key messages: </strong>A brief history on psycho-neuro-endocrine immunology cannot address all relevant aspects of the field. The authors are aware of this shortcoming. The reader must see this review as a viewpoint through the biased eyes of the authors. Nevertheless, the text gives an overview of the history in psycho-neuro-endocrine immunology of rheumatic diseases.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"183-210"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142018157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-08-08DOI: 10.1159/000540460
Qi Tian, Ziang Yan, Yujia Guo, Zhibiao Chen, Mingchang Li
Background: Chemokine ligands and their corresponding receptors are essential for regulating inflammatory responses. Chemokine receptors can stimulate immune activation or inhibit/promote signaling pathways by binding to specific chemokine ligands. Among these receptors, CC chemokine receptor 1 (CCR1) is extensively studied as a G protein-linked receptor target, predominantly expressed in various leukocytes, and is considered a promising target for anti-inflammatory therapy. Furthermore, CCR1 is essential for monocyte extravasation and transportation in inflammatory conditions. Its involvement in inflammatory diseases of the central nervous system (CNS), including multiple sclerosis, Alzheimer's disease, and stroke, has been extensively studied along with its ligands. Animal models have demonstrated the beneficial effects resulting from inhibiting CCR1 or its ligands.
Summary: This review demonstrates the significance of CCR1 in CNS inflammatory diseases, the molecules implicated in the inflammatory pathway, and potential drugs or molecules for treating CNS diseases. This evidence may offer new targets or strategies for treating inflammatory CNS diseases.
{"title":"Inflammatory Role of CCR1 in the Central Nervous System.","authors":"Qi Tian, Ziang Yan, Yujia Guo, Zhibiao Chen, Mingchang Li","doi":"10.1159/000540460","DOIUrl":"10.1159/000540460","url":null,"abstract":"<p><strong>Background: </strong>Chemokine ligands and their corresponding receptors are essential for regulating inflammatory responses. Chemokine receptors can stimulate immune activation or inhibit/promote signaling pathways by binding to specific chemokine ligands. Among these receptors, CC chemokine receptor 1 (CCR1) is extensively studied as a G protein-linked receptor target, predominantly expressed in various leukocytes, and is considered a promising target for anti-inflammatory therapy. Furthermore, CCR1 is essential for monocyte extravasation and transportation in inflammatory conditions. Its involvement in inflammatory diseases of the central nervous system (CNS), including multiple sclerosis, Alzheimer's disease, and stroke, has been extensively studied along with its ligands. Animal models have demonstrated the beneficial effects resulting from inhibiting CCR1 or its ligands.</p><p><strong>Summary: </strong>This review demonstrates the significance of CCR1 in CNS inflammatory diseases, the molecules implicated in the inflammatory pathway, and potential drugs or molecules for treating CNS diseases. This evidence may offer new targets or strategies for treating inflammatory CNS diseases.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"173-182"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141907224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2023-12-21DOI: 10.1159/000535859
Carolina Francelin, Alexandre Borin, Jessica Funari, Fernando Pradella, Leonilda M B Santos, Wilson Savino, Alessandro S Farias
Introduction: The thymus is the primary lymphoid organ responsible for normal T-cell development. Yet, in abnormal metabolic conditions as well as an acute infection, the organ exhibits morphological and cellular alterations. It is well established that the immune system is in a tidy connection and dependent on the central nervous system (CNS), which regulates thymic function by means of innervation and neurotransmitters. Sympathetic innervation leaves the CNS and spreads through thymic tissue, where nerve endings interact directly or indirectly with thymic cells contributing to their maintenance and development.
Methods: Herein, we hypothesized that brain damage due to an inflammatory process might elicit alterations upon the thymic-CNS neuroimmune axis, altering not just the sympathetic innervation and neurotransmitter release, but also modifying the thymus microenvironment and T-cell development. We used the well-established multiple sclerosis model of experimental autoimmune encephalomyelitis (EAE), to study putative changes in the thymic neural, lymphoid, and microenvironmental compartments.
Results: We showed that along with EAE clinical development, thymus morphology, and cellular compartments are affected, altering the peripheric T-cell population and modifying the retrograde thymic communication toward the CNS.
Conclusion: Altogether, our data suggest that the thymic-CNS neuroimmune bidirectional axis is compromised in EAE. This imbalance may contribute to an increased and uncontrolled auto-immune reaction.
胸腺是负责 T 细胞正常发育的主要淋巴器官。然而,在代谢异常和急性感染的情况下,该器官会出现形态和细胞改变。众所周知,免疫系统与中枢神经系统(CNS)有着紧密的联系和依赖关系,中枢神经系统通过神经支配和神经递质调节胸腺功能。交感神经支配离开中枢神经系统,通过胸腺组织传播,神经末梢直接或间接地与胸腺细胞相互作用,促进胸腺细胞的维持和发育。在此,我们假设炎症过程导致的脑损伤可能会引起胸腺-中枢神经系统神经免疫轴的改变,不仅改变交感神经支配和神经递质的释放,还会改变胸腺微环境和T细胞的发育。我们利用实验性自身免疫性脑脊髓炎(EAE)这一成熟的多发性硬化症模型,研究了胸腺神经、淋巴和微环境的可能变化。我们发现,随着EAE临床发展,胸腺形态和细胞区受到影响,外周T细胞群发生改变,胸腺向中枢神经系统的逆行通讯也发生改变。总之,我们的数据表明,胸腺-中枢神经系统神经免疫双向轴在 EAE 中受到损害。这种失衡可能会导致自身免疫反应的加剧和失控。
{"title":"Thymic Innervation Impairment in Experimental Autoimmune Encephalomyelitis.","authors":"Carolina Francelin, Alexandre Borin, Jessica Funari, Fernando Pradella, Leonilda M B Santos, Wilson Savino, Alessandro S Farias","doi":"10.1159/000535859","DOIUrl":"10.1159/000535859","url":null,"abstract":"<p><strong>Introduction: </strong>The thymus is the primary lymphoid organ responsible for normal T-cell development. Yet, in abnormal metabolic conditions as well as an acute infection, the organ exhibits morphological and cellular alterations. It is well established that the immune system is in a tidy connection and dependent on the central nervous system (CNS), which regulates thymic function by means of innervation and neurotransmitters. Sympathetic innervation leaves the CNS and spreads through thymic tissue, where nerve endings interact directly or indirectly with thymic cells contributing to their maintenance and development.</p><p><strong>Methods: </strong>Herein, we hypothesized that brain damage due to an inflammatory process might elicit alterations upon the thymic-CNS neuroimmune axis, altering not just the sympathetic innervation and neurotransmitter release, but also modifying the thymus microenvironment and T-cell development. We used the well-established multiple sclerosis model of experimental autoimmune encephalomyelitis (EAE), to study putative changes in the thymic neural, lymphoid, and microenvironmental compartments.</p><p><strong>Results: </strong>We showed that along with EAE clinical development, thymus morphology, and cellular compartments are affected, altering the peripheric T-cell population and modifying the retrograde thymic communication toward the CNS.</p><p><strong>Conclusion: </strong>Altogether, our data suggest that the thymic-CNS neuroimmune bidirectional axis is compromised in EAE. This imbalance may contribute to an increased and uncontrolled auto-immune reaction.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"25-39"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138830752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-01-12DOI: 10.1159/000536204
Rainer H Straub, Dario Boschiero
Introduction: Patients often go to the physician with medically unexplained symptoms (MUS). MUS can be autonomic nervous system-related "unspecific" symptoms, such as palpitations, heart rhythm alterations, temperature dysregulation (hand, feet), anxiety, or depressive manifestations, fatigue, somnolence, nausea, hyperalgesia with varying pains and aches, dizziness, etc. Methods: In this real-world study, we investigated MUS in a cohort of unselected outpatients from general practitioners in Italy. It was our aim to increase the understanding of MUS by using principal component analyses to identify any subcategories of MUS and to check a role of chronic inflammatory diseases. Additionally, we studied cerebral blood oxygen (rCBO2) and associations with MUS and chronic inflammatory disease.
Results: Participants included 1,597 subjects (50.6 ± 0.4 years, 65%/35% women/men). According to ICD-10 codes, 137 subjects had chronic inflammatory diseases. MUS were checked by a questionnaire with a numeric rating scale and cerebral blood flow with optical techniques. The analyses of men and women were stratified. Psychological symptom severity was higher in the inflamed compared to the non-inflamed group (fatigue, insomnia in women and men; recent mood changes, daytime sleepiness, anxiety, apathy, cold hands only in women; abnormal appetite and heart rhythm problems only in men). Principal component analysis with MUS provided new subcategories: brain symptoms, gut symptoms, and unspecific symptoms. Brain and gut symptoms were higher in inflamed women and men. Chronic inflammatory diseases and pain were tightly interrelated in men and women (p < 0.0001). In women, not in men, average frontal rCBO2 content was higher in inflamed compared to non-inflamed subjects. In men, not in women, individuals with pain demonstrated a lower average frontal rCBO2 content compared to pain-free men. MUS did not relate to rCBO2 parameters.
Conclusion: This study shows close relationships between MUS and chronic inflammatory diseases but not between MUS and rCBO2 parameters.
{"title":"Medically Unexplained Symptoms Are Linked to Chronic Inflammatory Diseases: Is There a Role for Frontal Cerebral Blood Oxygen Content?","authors":"Rainer H Straub, Dario Boschiero","doi":"10.1159/000536204","DOIUrl":"10.1159/000536204","url":null,"abstract":"<p><strong>Introduction: </strong>Patients often go to the physician with medically unexplained symptoms (MUS). MUS can be autonomic nervous system-related \"unspecific\" symptoms, such as palpitations, heart rhythm alterations, temperature dysregulation (hand, feet), anxiety, or depressive manifestations, fatigue, somnolence, nausea, hyperalgesia with varying pains and aches, dizziness, etc. Methods: In this real-world study, we investigated MUS in a cohort of unselected outpatients from general practitioners in Italy. It was our aim to increase the understanding of MUS by using principal component analyses to identify any subcategories of MUS and to check a role of chronic inflammatory diseases. Additionally, we studied cerebral blood oxygen (rCBO2) and associations with MUS and chronic inflammatory disease.</p><p><strong>Results: </strong>Participants included 1,597 subjects (50.6 ± 0.4 years, 65%/35% women/men). According to ICD-10 codes, 137 subjects had chronic inflammatory diseases. MUS were checked by a questionnaire with a numeric rating scale and cerebral blood flow with optical techniques. The analyses of men and women were stratified. Psychological symptom severity was higher in the inflamed compared to the non-inflamed group (fatigue, insomnia in women and men; recent mood changes, daytime sleepiness, anxiety, apathy, cold hands only in women; abnormal appetite and heart rhythm problems only in men). Principal component analysis with MUS provided new subcategories: brain symptoms, gut symptoms, and unspecific symptoms. Brain and gut symptoms were higher in inflamed women and men. Chronic inflammatory diseases and pain were tightly interrelated in men and women (p < 0.0001). In women, not in men, average frontal rCBO2 content was higher in inflamed compared to non-inflamed subjects. In men, not in women, individuals with pain demonstrated a lower average frontal rCBO2 content compared to pain-free men. MUS did not relate to rCBO2 parameters.</p><p><strong>Conclusion: </strong>This study shows close relationships between MUS and chronic inflammatory diseases but not between MUS and rCBO2 parameters.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"40-50"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139466832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-02-16DOI: 10.1159/000536419
Daniella Arêas Mendes-da-Cruz, Elizabeth Pinto Belorio, Vinicius Cotta-de-Almeida
Background: T-cell acute lymphoblastic leukemia (T-ALL) is a malignant hematologic disease caused by the transformation and uncontrolled proliferation of T-cell precursors. T-ALL is generally thought to originate in the thymus since lymphoblasts express phenotypic markers comparable to those described in thymocytes in distinct stages of development. Although around 50% of T-ALL patients present a thymic mass, T-ALL is characterized by peripheral blood and bone marrow involvement, and central nervous system (CNS) infiltration is one of the most severe complications of the disease.
Summary: The CNS invasion is related to the expression of specific adhesion molecules and receptors commonly expressed in developing T cells, such as L-selectin, CD44, integrins, and chemokine receptors. Furthermore, T-ALL blasts also express neurotransmitters, neuropeptides, and cognate receptors that are usually present in the CNS and can affect both the brain and thymus, participating in the crosstalk between the organs.
Key messages: This review discusses how the thymus-brain connections, mediated by innervation and common molecules and receptors, can impact the development and migration of T-ALL blasts, including CNS infiltration.
背景:T 细胞急性淋巴细胞白血病(T-ALL)是一种恶性血液病,由 T 细胞前体转化和不受控制的增殖引起。一般认为 T-ALL 起源于胸腺,因为淋巴母细胞表达的表型标记与处于不同发育阶段的胸腺细胞所表达的表型标记相似。虽然约 50%的 T-ALL 患者出现胸腺肿块,但 T-ALL 的特点是外周血和骨髓受累,中枢神经系统(CNS)浸润是该病最严重的并发症之一。摘要:CNS 侵袭与发育中的 T 细胞通常表达的特定粘附分子和受体有关,如 L-选择素、CD44、整合素和趋化因子受体。此外,T-ALL 血块还表达通常存在于中枢神经系统的神经递质、神经肽和同源受体,并可影响大脑和胸腺,参与器官间的串联:这篇综述讨论了胸腺与大脑之间的联系如何通过神经支配、共同分子和受体介导,影响T-ALL胚泡的发育和迁移,包括中枢神经系统浸润。
{"title":"Thymus-Brain Connections in T-Cell Acute Lymphoblastic Leukemia.","authors":"Daniella Arêas Mendes-da-Cruz, Elizabeth Pinto Belorio, Vinicius Cotta-de-Almeida","doi":"10.1159/000536419","DOIUrl":"10.1159/000536419","url":null,"abstract":"<p><strong>Background: </strong>T-cell acute lymphoblastic leukemia (T-ALL) is a malignant hematologic disease caused by the transformation and uncontrolled proliferation of T-cell precursors. T-ALL is generally thought to originate in the thymus since lymphoblasts express phenotypic markers comparable to those described in thymocytes in distinct stages of development. Although around 50% of T-ALL patients present a thymic mass, T-ALL is characterized by peripheral blood and bone marrow involvement, and central nervous system (CNS) infiltration is one of the most severe complications of the disease.</p><p><strong>Summary: </strong>The CNS invasion is related to the expression of specific adhesion molecules and receptors commonly expressed in developing T cells, such as L-selectin, CD44, integrins, and chemokine receptors. Furthermore, T-ALL blasts also express neurotransmitters, neuropeptides, and cognate receptors that are usually present in the CNS and can affect both the brain and thymus, participating in the crosstalk between the organs.</p><p><strong>Key messages: </strong>This review discusses how the thymus-brain connections, mediated by innervation and common molecules and receptors, can impact the development and migration of T-ALL blasts, including CNS infiltration.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"51-61"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139564610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-03-12DOI: 10.1159/000538294
Carsten Schradin, Adrian V Jaeggi, Francois Criscuolo
Background: Evolutionary medicine builds on evolutionary biology and explains why natural selection has left us vulnerable to disease. Unfortunately, several misunderstandings exist in the medical literature about the levels and mechanisms of evolution. Reasons for these problems start from the lack of teaching evolutionary biology in medical schools. A common mistake is to assume that "traits must benefit the species, as otherwise the species would have gone extinct in the past" confusing evolutionary history (phylogeny) with evolutionary function (fitness).
Summary: Here we summarise some basic aspects of evolutionary medicine by pointing out: (1) Evolution has no aim. (2) For adaptive evolution to occur, a trait does not have to be beneficial to its carrier throughout its entire life. (3) Not every single individual carrying an adaptive trait needs to have higher than average fitness. (4) Traits do not evolve for the benefit of the species. Using examples from the field of neuroimmunomodulation like sickness behaviour (nervous system), testosterone (hormones), and cytokines (immunity), we show how misconceptions arise from not differentiating between the explanatory categories of phylogeny (evolutionary history) and evolutionary function (fitness).
Key messages: Evolution has no aim but is an automatism that does not function for the benefit of the species. In evolution, successful individuals are those that maximise the transmission of their genes, and health and survival are just strategies to have the opportunity to do so. Thus, a trait enabling survival of the individual until reproductive age will spread even if at later age the same trait leads to disease and death. Natural and sexual selection do not select for traits that benefit the health or happiness of the individual, but for traits that increase inclusive fitness even if this increases human suffering. In contrast, our humane aim is to increase individual well-being. Evolutionary medicine can help us achieve this aim against evolutionary constraints.
{"title":"Quick Guide to Evolutionary Medicine in Neuroimmunomodulation: Why \"Evolved for the Benefit of the Species\" Is Not a Valid Argument.","authors":"Carsten Schradin, Adrian V Jaeggi, Francois Criscuolo","doi":"10.1159/000538294","DOIUrl":"10.1159/000538294","url":null,"abstract":"<p><strong>Background: </strong>Evolutionary medicine builds on evolutionary biology and explains why natural selection has left us vulnerable to disease. Unfortunately, several misunderstandings exist in the medical literature about the levels and mechanisms of evolution. Reasons for these problems start from the lack of teaching evolutionary biology in medical schools. A common mistake is to assume that \"traits must benefit the species, as otherwise the species would have gone extinct in the past\" confusing evolutionary history (phylogeny) with evolutionary function (fitness).</p><p><strong>Summary: </strong>Here we summarise some basic aspects of evolutionary medicine by pointing out: (1) Evolution has no aim. (2) For adaptive evolution to occur, a trait does not have to be beneficial to its carrier throughout its entire life. (3) Not every single individual carrying an adaptive trait needs to have higher than average fitness. (4) Traits do not evolve for the benefit of the species. Using examples from the field of neuroimmunomodulation like sickness behaviour (nervous system), testosterone (hormones), and cytokines (immunity), we show how misconceptions arise from not differentiating between the explanatory categories of phylogeny (evolutionary history) and evolutionary function (fitness).</p><p><strong>Key messages: </strong>Evolution has no aim but is an automatism that does not function for the benefit of the species. In evolution, successful individuals are those that maximise the transmission of their genes, and health and survival are just strategies to have the opportunity to do so. Thus, a trait enabling survival of the individual until reproductive age will spread even if at later age the same trait leads to disease and death. Natural and sexual selection do not select for traits that benefit the health or happiness of the individual, but for traits that increase inclusive fitness even if this increases human suffering. In contrast, our humane aim is to increase individual well-being. Evolutionary medicine can help us achieve this aim against evolutionary constraints.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"66-77"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140110887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-10-04DOI: 10.1159/000541592
Alexander M Kuhn, Kelly E Bosis, Eric S Wohleb
Background: From the original studies investigating the effects of adrenal gland secretion to modern high-throughput multidimensional analyses, stress research has been a topic of scientific interest spanning just over a century.
Summary: The objective of this review was to provide historical context for influential discoveries, surprising findings, and preclinical models in stress-related neuroimmune research. Furthermore, we summarize this work and present a current understanding of the stress pathways and their effects on the immune system and behavior. We focus on recent work demonstrating stress-induced immune changes within the brain and highlight studies investigating stress effects on microglia. Lastly, we conclude with potential areas for future investigation concerning microglia heterogeneity, bone marrow niches, and sex differences.
Key messages: Stress is a phenomenon that ties together not only the central and peripheral nervous system, but the immune system as well. The cumulative effects of stress can enhance or suppress immune function, based on the intensity and duration of the stressor. These stress-induced immune alterations are associated with neurobiological changes, including structural remodeling of neurons and decreased neurogenesis, and these contribute to the development of behavioral and cognitive deficits. As such, research in this field has revealed important insights into neuroimmune communication as well as molecular and cellular mediators of complex behaviors relevant to psychiatric disorders.
{"title":"Looking Back to Move Forward: Research in Stress, Behavior, and Immune Function.","authors":"Alexander M Kuhn, Kelly E Bosis, Eric S Wohleb","doi":"10.1159/000541592","DOIUrl":"10.1159/000541592","url":null,"abstract":"<p><strong>Background: </strong>From the original studies investigating the effects of adrenal gland secretion to modern high-throughput multidimensional analyses, stress research has been a topic of scientific interest spanning just over a century.</p><p><strong>Summary: </strong>The objective of this review was to provide historical context for influential discoveries, surprising findings, and preclinical models in stress-related neuroimmune research. Furthermore, we summarize this work and present a current understanding of the stress pathways and their effects on the immune system and behavior. We focus on recent work demonstrating stress-induced immune changes within the brain and highlight studies investigating stress effects on microglia. Lastly, we conclude with potential areas for future investigation concerning microglia heterogeneity, bone marrow niches, and sex differences.</p><p><strong>Key messages: </strong>Stress is a phenomenon that ties together not only the central and peripheral nervous system, but the immune system as well. The cumulative effects of stress can enhance or suppress immune function, based on the intensity and duration of the stressor. These stress-induced immune alterations are associated with neurobiological changes, including structural remodeling of neurons and decreased neurogenesis, and these contribute to the development of behavioral and cognitive deficits. As such, research in this field has revealed important insights into neuroimmune communication as well as molecular and cellular mediators of complex behaviors relevant to psychiatric disorders.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"211-229"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-01-01Epub Date: 2024-05-02DOI: 10.1159/000539073
Manfred Schedlowski, Martin Hadamitzky
Background: More than a century ago, experimental work and clinical observations revealed the functional communication between the brain and the peripheral immune system. This is documented on the one hand by studies first demonstrating the effects of catecholamines on the circulation of leukocytes in experimental animals and humans, and on the other hand via the work of Russian physiologist Ivan Petrovic Pavlov and his coworkers, reporting observations that associative learning can modify peripheral immune functions. This work later fell into oblivion since little was known about the endocrine and immune system's function and even less about the underlying mechanisms of how learning, a central nervous system activity, could affect peripheral immune responses.
Summary: In this article, we embark on a fascinating exploration of the historical trajectory of behaviorally conditioned immune responses.
Key message: We will pay homage to the visionary scientists who laid the groundwork for this field of research, tracing its evolution from early theories of how associative learning can affect immunity to the modern-day insights that behavioral conditioning of pharmacological responses can be exploited to improve the efficacy of medical interventions for patients.
{"title":"Behaviorally Conditioned Immune Responses: \"To Learn New Things, Read Old Books and Papers\".","authors":"Manfred Schedlowski, Martin Hadamitzky","doi":"10.1159/000539073","DOIUrl":"10.1159/000539073","url":null,"abstract":"<p><strong>Background: </strong>More than a century ago, experimental work and clinical observations revealed the functional communication between the brain and the peripheral immune system. This is documented on the one hand by studies first demonstrating the effects of catecholamines on the circulation of leukocytes in experimental animals and humans, and on the other hand via the work of Russian physiologist Ivan Petrovic Pavlov and his coworkers, reporting observations that associative learning can modify peripheral immune functions. This work later fell into oblivion since little was known about the endocrine and immune system's function and even less about the underlying mechanisms of how learning, a central nervous system activity, could affect peripheral immune responses.</p><p><strong>Summary: </strong>In this article, we embark on a fascinating exploration of the historical trajectory of behaviorally conditioned immune responses.</p><p><strong>Key message: </strong>We will pay homage to the visionary scientists who laid the groundwork for this field of research, tracing its evolution from early theories of how associative learning can affect immunity to the modern-day insights that behavioral conditioning of pharmacological responses can be exploited to improve the efficacy of medical interventions for patients.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"102-113"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140860978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}