Neuroimmunomodulation最新文献

{"title":"Cytokines in Cerebrospinal Fluid and Chronic Pain in Humans: Past, Present, and Future.","authors":"Alexander H C Rosenström, Jan-Pieter Konsman, Eva Kosek","doi":"10.1159/000540324","DOIUrl":"10.1159/000540324","url":null,"abstract":"<p><strong>Background: </strong>That neuroimmune interaction occurs in chronic pain conditions has been established for over a century, since the discovery of neurogenic inflammation in the periphery. However, the central aspects of neuroimmune interactions have not been fully appreciated until the late 1900s, when a growing interest in how cytokines in the cerebrospinal fluid (CSF) might be relevant in chronic pain conditions emerged. Since then, the field has evolved, and nowadays neuroinflammation is considered to be involved in the pathophysiology of chronic pain. Whether or not pain conditions can be called \"neuroinflammatory\" is a matter of debate. This review summarizes the results from studies investigating cytokines in the CSF in various pain conditions, and critically discusses neuroimmune aspects of pain conditions using previously proposed hallmarks of neuroinflammation as a framework.</p><p><strong>Summary: </strong>Fifty-two papers were summarized and their results evaluated according to (a) the level of the measured cytokines in patients compared to controls, and (b) the correlation between cytokine level and pain intensity. A subdivision based on pain type was also conducted for each of the 52 studies. A total of 49 proteins have been studied in at least 5 studies, 21 of which were upregulated in a majority of studies. IL-8 was specifically upregulated in a majority of studies of nociceptive pain conditions. Regarding correlation to pain intensity, there is a scarcity of data but 31 proteins were upregulated and correlated with pain in at least one study. Of these, 24 proteins were negatively correlated with pain, and 7 were positively correlated. None of the most studied cytokines, such as TNF, IL-1b, IL-6, IL-8, CCL2/MCP1, BDNF, or bNGF, were consistently correlated to pain.</p><p><strong>Key messages: </strong>There is sufficient evidence to say that chronic pain conditions come with an upregulation of several cytokines. However, the majority of correlations to symptomatology seem to be negative, indicating that the cytokines might play a protective role that has not been broadly considered. Calling chronic pain conditions neuroinflammatory seems wrong; instead, a more suitable term for depicting the findings would, perhaps, be to talk about neuroimmune activation.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"157-172"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141620427","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}

{"title":"2nd European Psychoneuroimmunology Network (EPN) Autumn School: The skin-brain axis and the breaking of barriers","authors":"","doi":"10.1159/000533642","DOIUrl":"https://doi.org/10.1159/000533642","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"30 1","pages":"1 - 2"},"PeriodicalIF":2.4,"publicationDate":"2023-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46142806","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}

{"title":"2nd European Psychoneuroimmunology Network Autumn School: The Skin-Brain Axis and the Breaking of Barriers.","authors":"Eva Peters,&nbsp;Adriana Del Rey,&nbsp;Karsten Krüger,&nbsp;Christoph Rummel","doi":"10.1159/000533611","DOIUrl":"10.1159/000533611","url":null,"abstract":"aDepartment of Psychosomatic Medicine and Psychotherapy, Psychoneuroimmunology Laboratory, Justus-Liebig University Giessen, Giessen, And Universitätsmedizin-Charité, Berlin, Germany; bCenter for Mind, Brain and Behavior (CMBB), University of Marburg and Justus Liebig University Giessen, Marburg, Germany; cInstitute for Physiology and Pathophysiology, University of Marburg, Marburg, Germany; dDepartment of Exercise Physiology and Sports Therapy, Justus Liebig University Giessen, Giessen, Germany; eInstitute of Veterinary Physiology and Biochemistry, Justus Liebig University Giessen, Giessen, Germany","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"30 Suppl 1 ","pages":"3-7"},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10627488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10109350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum.","authors":"","doi":"10.1159/000531806","DOIUrl":"10.1159/000531806","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"30 1","pages":"213-214"},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10308955","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}

{"title":"15th Conference of the German Endocrine-Brain- Immune-Network (GEBIN) Ulm, Germany, September 28 - September 30, 2023.","authors":"","doi":"10.1159/000533771","DOIUrl":"10.1159/000533771","url":null,"abstract":"The abstracts included in this supplement were reviewed and selected by the Scientific Programme Committee. The committee has no conflicts of interest in connection with the congress and the selection of abstracts. Neuroimmunomodulation 2023;30(suppl 2):1–60 DOI: 10.1159/000533771 Published online: September 19, 2023 This article is licensed under the Creative Commons AttributionNonCommercial 4.0 International License (CCBY-NC) (http://www. karger.com/Services/OpenAccessLicense).Usage anddistribution for commercial purposes requires written permission.","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":"30 Suppl 2 ","pages":"1-60"},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41109584","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}

{"title":"Understanding the Immune-Endocrine Effects of Vitamin D in SARS-CoV-2 Infection: A Role in Protecting against Neurodamage.","authors":"Emanuele Gotelli, Stefano Soldano, Elvis Hysa, Andrea Casabella, Andrea Cere, Carmen Pizzorni, Sabrina Paolino, Alberto Sulli, Vanessa Smith, Maurizio Cutolo","doi":"10.1159/000533286","DOIUrl":"10.1159/000533286","url":null,"abstract":"<p><p>Calcitriol and hydroxyderivatives of lumisterol and tachisterol are secosteroid hormones with immunomodulatory and anti-inflammatory properties. Since the beginning of the COVID-19 pandemic, several studies have correlated deficient serum concentrations of vitamin D3 (calcifediol) with increased severity of the course of SARS-CoV-2 infection. Among systemic complications, subjective (anosmia, ageusia, depression, dizziness) and objective (ischemic stroke, meningoencephalitis, myelitis, seizures, Guillain-Barré syndrome) neurological symptoms have been reported in up to 80% of severe COVID-19 patients. In this narrative review, we will resume the pathophysiology of SARS-CoV-2 infection and the mechanisms of acute and chronic neurological damage. SARS-CoV-2 can disrupt the integrity of the endothelial cells of the blood-brain barrier (BBB) to enter the nervous central system. Invasion of pro-inflammatory cytokines and polarization of astrocytes and microglia cells always in a pro-inflammatory sense together with the pro-coagulative phenotype of cerebral endothelial cells in response to both SARS-CoV-2 and immune cells invasion (immunothrombosis) are the major drivers of neurodamage. Calcitriol and hydroxyderivatives of lumisterol and tachisterol could play an adjuvant role in neuroprotection through mitigation of neuroinflammation and protection of endothelial integrity of the BBB. Dedicated studies on this topic are currently lacking and are desirable to confirm the link between vitamin D3 and neuroprotection in COVID-19 patients.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"185-195"},"PeriodicalIF":2.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614436/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10319984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuropsychiatric Outcomes and Sleep Dysfunction in COVID-19 Patients: Risk Factors and Mechanisms.","authors":"Aliki Karkala, Asterios Tzinas, Seraphim Kotoulas, Athanasios Zacharias, Evdokia Sourla, Athanasia Pataka","doi":"10.1159/000533722","DOIUrl":"10.1159/000533722","url":null,"abstract":"<p><p>The ongoing global health crisis due to the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has significantly impacted all aspects of life. While the majority of early research following the coronavirus disease caused by SARS-CoV-2 (COVID-19) has focused on the physiological effects of the virus, a substantial body of subsequent studies has shown that the psychological burden of the infection is also considerable. Patients, even without mental illness history, were at increased susceptibility to developing mental health and sleep disturbances during or after the COVID-19 infection. Viral neurotropism and inflammatory storm damaging the blood-brain barrier have been proposed as possible mechanisms for mental health manifestations, along with stressful psychological factors and indirect consequences such as thrombosis and hypoxia. The virus has been found to infect peripheral olfactory neurons and exploit axonal migration pathways, exhibiting metabolic changes in astrocytes that are detrimental to fueling neurons and building neurotransmitters. Patients with COVID-19 present dysregulated and overactive immune responses, resulting in impaired neuronal function and viability, adversely affecting sleep and emotion regulation. Additionally, several risk factors have been associated with the neuropsychiatric sequelae of the infection, such as female sex, age, preexisting neuropathologies, severity of initial disease and sociological status. This review aimed to provide an overview of mental health symptoms and sleep disturbances developed during COVID-19 and to analyze the underlying mechanisms and risk factors of psychological distress and sleep dysfunction.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"237-249"},"PeriodicalIF":2.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41105282","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}

{"title":"Endotoxin-Induced Physiological and Psychological Sickness Responses in Healthy Humans: Insights into the Post-Acute Phase.","authors":"Harald Engler, Alexandra Brinkhoff, Benjamin Wilde, Andreas Kribben, Hana Rohn, Oliver Witzke, Manfred Schedlowski, Sven Benson","doi":"10.1159/000534444","DOIUrl":"10.1159/000534444","url":null,"abstract":"<p><strong>Introduction: </strong>Experimental endotoxemia is a translational model of systemic inflammation that has contributed significantly to our current understanding of sickness behavior and inflammation-associated depression. Previous studies using this model revealed a strong association between cytokine levels, endocrine changes, and psychological sickness symptoms during the acute phase of inflammation. The objective of this randomized, double-blind, placebo-controlled crossover study was to gain insight into potential post-acute physiological and psychological consequences of endotoxin administration that may either persist or newly emerge between 24 and 72 h after injection. The main focus was on associations between serum levels of C-reactive protein (CRP) and affective symptoms as well as alterations in diurnal cortisol profile, the two key features of inflammation-associated depression.</p><p><strong>Methods: </strong>Healthy male volunteers (N = 18) received an injection of either endotoxin (0.8 ng/kg) or placebo on two separate but otherwise identical study days, 7 days apart. Blood and saliva samples were collected during acute and post-acute phases after injection to measure blood inflammatory markers (interleukin [IL]-6, IL-1 receptor antagonist [ra], CRP) and salivary cortisol levels. In addition, participants completed a comprehensive battery of questionnaires to assess physical and psychological sickness symptoms.</p><p><strong>Results: </strong>Endotoxin treatment induced a short-time rise in plasma IL-6 and a longer increase in IL-1ra. The increase in serum CRP was delayed compared to cytokines, peaking at 24 h and gradually decreasing until 72 h after injection. The inflammatory response was accompanied by bodily and psychological sickness symptoms which occurred only in the acute phase, whereas none of the symptoms persisted or recurred in the post-acute phase. Salivary cortisol levels were significantly increased during the acute phase and exhibited pronounced circadian changes. However, no significant differences in diurnal cortisol profiles were observed between placebo and endotoxin conditions on the days after treatment.</p><p><strong>Conclusion: </strong>Our findings suggest that CRP, which is elevated in patients with inflammation-associated depression, does not appear to be responsible for depressive symptomatology. Moreover, a single inflammatory episode is not sufficient to alter diurnal cortisol profiles, as observed in inflammation-associated depression. In addition, the absence of persistent lipopolysaccharide-induced psychological and physiological changes beyond the acute phase further supports the safety of endotoxin administration in humans.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"268-276"},"PeriodicalIF":2.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10623394/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41129809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Vagus Nerve Stimulation in the Treatment of Chronic Pain.","authors":"Peiqi Shao, Huili Li, Jia Jiang, Yun Guan, Xueming Chen, Yun Wang","doi":"10.1159/000531626","DOIUrl":"10.1159/000531626","url":null,"abstract":"<p><p>Vagus nerve stimulation (VNS) can modulate vagal activity and neuro-immune communication. Human and animal studies have provided growing evidence that VNS can produce analgesic effects in addition to alleviating refractory epilepsy and depression. The vagus nerve (VN) projects to many brain regions related to pain processing, which can be affected by VNS. In addition to neural regulation, the anti-inflammatory property of VNS may also contribute to its pain-inhibitory effects. To date, both invasive and noninvasive VNS devices have been developed, with noninvasive devices including transcutaneous stimulation of auricular VN or carotid VN that are undergoing many clinical trials for chronic pain treatment. This review aimed to provide an update on both preclinical and clinical studies of VNS in the management for chronic pain, including fibromyalgia, abdominal pain, and headaches. We further discuss potential underlying mechanisms for VNS to inhibit chronic pain.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"167-183"},"PeriodicalIF":2.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10614462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9695915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Effects of the Sympathetic Nervous System in Inflammatory Models.","authors":"Georg Pongratz, Rainer H Straub","doi":"10.1159/000530969","DOIUrl":"10.1159/000530969","url":null,"abstract":"<p><p>The immune system is embedded in a network of regulatory systems to keep homeostasis in case of an immunologic challenge. Neuroendocrine immunologic research has revealed several aspects of these interactions over the past decades, e.g., between the autonomic nervous system and the immune system. This review will focus on evidence revealing the role of the sympathetic nervous system (SNS) in chronic inflammation, like colitis, multiple sclerosis, systemic sclerosis, lupus erythematodes, and arthritis with a focus on animal models supported by human data. A theory of the contribution of the SNS in chronic inflammation will be presented that spans these disease entities. One major finding is the biphasic nature of the sympathetic contribution to inflammation, with proinflammatory effects until the point of disease outbreak and mainly anti-inflammatory influence thereafter. Since sympathetic nerve fibers are lost from sites of inflammation during inflammation, local cells and immune cells achieve the capability to endogenously produce catecholamines to fine-tune the inflammatory response independent of brain control. On a systemic level, it has been shown across models that the SNS is activated in inflammation as opposed to the parasympathetic nervous system. Permanent overactivity of the SNS contributes to many of the known disease sequelae. One goal of neuroendocrine immune research is defining new therapeutic targets. In this respect, it will be discussed that at least in arthritis, it might be beneficial to support β-adrenergic and inhibit α-adrenergic activity besides restoring autonomic balance. Overall, in the clinical setting, we now need controlled interventional studies to successfully translate the theoretical knowledge into benefits for patients.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"113-134"},"PeriodicalIF":2.2,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9893291","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}