Neuroimmunomodulation最新文献

{"title":"Why Differences in Methods and Resulting Misinterpretation of Telomere Data Might Affect Our Perspective on Aging and Its Reversibility by Clinical Interventions.","authors":"Alexander Karabatsiakis","doi":"10.1159/000549809","DOIUrl":"10.1159/000549809","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"1-4"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12774421/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145648972","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":"<italic>Mycobacterium vaccae</italic> NCTC 11659 Attenuates Early Life Adversity-Induced Hippocampal Neuroinflammation in Mice.","authors":"Tamara Schimmele, Nina M Castaneda, Giulia Mazzari, Laura K Fonken, Stefan O Reber","doi":"10.1159/000552593","DOIUrl":"10.1159/000552593","url":null,"abstract":"<p><strong>Introduction: </strong>Early life adversity (ELA) is a potent risk factor for negative mental health outcomes, in part through its enduring effects on neuroimmune function. The hippocampus is particularly sensitive to stress across the lifespan, and neuroinflammatory signaling has been implicated as a mediator linking a life stress history to vulnerability. Accordingly, we hypothesized that ELA, in particular when followed by chronic psychosocial stress during adulthood (CAS), would enhance expression of inflammatory genes in the hippocampus and that these effects would be ameliorated by intervention with Mycobacterium vaccae (M. vaccae), a soil-derived mycobacterium with immunoregulatory properties.</p><p><strong>Methods: </strong>To test this, newborn male and female mice were exposed to the maternal separation (MS) paradigm between postnatal days (PNDs) 1-14 (i.e., 3h/day) before receiving repeated (3x) weekly (i.e., starting 1-2 weeks following weaning) subcutaneous (s.c.) administrations with sterile borate-buffered saline (BBS) as vehicle or a heat-killed preparation of M. vaccae NCTC (National Collection of Type Cultures) 11659 (0.1 mg/0.1 mL per s.c. injection) in sterile BBS. At the age of 7-8 weeks, CAS was induced in males by the chronic subordinate colony housing (CSC) paradigm and in females by the social instability paradigm (SIP), before all mice were euthanized and hippocampal tissue was isolated by micropunch for RNA extraction and quantitative PCR analysis of neuroinflammatory markers.</p><p><strong>Results: </strong>Among the panel of genes assessed, ELA significantly increased hippocampal expression of Iba1, CCL2, and IL-1β in vehicle- but not M. vaccae NCTC 11659-administered male and female mice. Surprisingly, CAS exposure alone did not affect hippocampal gene expression and even abrogated the reported ELA-induced expression changes.</p><p><strong>Conclusion: </strong>Together, these findings highlight hippocampal neuroimmune pathways as a mechanism by which predominantly ELA shapes long-term vulnerability, and support M. vaccae NCTC 11659 as a promising strategy for mitigating ELA-induced neuroinflammation.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"278-287"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13332798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147988580","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":"Interactions between Innate Immune Memory and the Central Nervous System.","authors":"Rafaela Rodrigues Valerio, Andressa Bernardi, Adriana Bonomo, Rudimar Luiz Frozza","doi":"10.1159/000551784","DOIUrl":"10.1159/000551784","url":null,"abstract":"<p><strong>Background: </strong>Traditionally, immunology has assumed the dogma that immunological memory is exclusive to cells of the adaptive immune system. However, over the past decade, evidence has challenged this paradigm by demonstrating that innate immune cells can exhibit adaptive characteristics, resulting in long-term functional changes. After exposure to infections or sterile inflammation, innate immune cells can exhibit either an enhanced or suppressed inflammatory response upon secondary challenge. This de facto immune memory has been termed trained immunity or immune tolerance, respectively.</p><p><strong>Summary: </strong>This review outlines both classical and newly described features of innate immune cells, highlighting the concepts of trained immunity and innate tolerance, along with their underlying molecular mechanisms. We also discuss the implications of innate immune memory in microglia and explore the potential therapeutic approaches for manipulating innate immunity in the context of neurodegenerative disorders.</p><p><strong>Key messages: </strong>While trained immunity plays a crucial role in protecting the host against infections, its dysregulation can lead to chronic inflammation, autoimmune diseases, and potentially contribute to the development of neurodegenerative disorders. On the other hand, tolerance can reduce the inflammatory response and promote tissue regeneration but can also result in increased susceptibility to secondary infections. The long lifespan of microglia, coupled with their ability to learn and adapt their response to previously encountered pathogens or stimuli, underscores the potential long-term implications of their innate immune memory for the development of neuropathology.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"180-199"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581856","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":"Glial Cells as Central Players in Neuroinflammation and Neuronal Damage Caused by Bacterial Pneumonia.","authors":"Aléxia M S Ferreira, Léo Victor G Castro, Marina Ferreira-Costa, Cassiano F Gonçalves-de-Albuquerque, Adriana R Silva","doi":"10.1159/000550709","DOIUrl":"10.1159/000550709","url":null,"abstract":"<p><strong>Background: </strong>Pneumonia is an infection that affects the alveolar spaces of the lungs, associated with high global mortality, and remains a significant public health challenge worldwide. In a compromised immune system, the infection can progress, leading to the establishment of pneumonia. During this process, an intense inflammatory response is triggered in the lungs through the activation of resident immune cells, especially alveolar macrophages. This activation promotes the recruitment of neutrophils and the release of pro-inflammatory cytokines, ultimately resulting in the formation of exudative infiltrates within the alveoli. Pneumonia is a leading cause of sepsis, particularly among hospitalized patients and in intensive care units. Sepsis represents one of the most severe complications of pneumonia and is characterized by a dysregulated systemic inflammatory response to lung infection. Another critical challenge to treating clinical infectious conditions, which can lead to life-threatening sepsis, septic shock, and multiorgan dysfunction, is the continuous growth of antimicrobial resistance in bacteria.</p><p><strong>Summary: </strong>Among the organ dysfunctions associated with sepsis, sepsis-associated encephalopathy (SAE) is the most frequent and constitutes a primary contributor to the neurological alterations observed in critically ill patients. Although SAE is often classified as a fully reversible pathophysiological process, increasing evidence suggests an association between sepsis, structural brain injury, and long-term neurological sequelae. The central nervous system (CNS) is one of the first regions exposed to peripheral inflammation during sepsis, allowing inflammatory mediators and immune cells to infiltrate the brain. This process activates microglia, the resident immune cells of the CNS, exposing neurons to an oxidative stress-rich environment that leads to neuronal dysfunction and apoptosis. A dysregulated pro-inflammatory microglial response plays a significant role in SAE, as microglia-derived cytokines are strongly associated with neuronal damage. Furthermore, activated microglia stimulate astrocytes to adopt a reactive inflammatory phenotype, thereby amplifying neuroinflammation.</p><p><strong>Key messages: </strong>Recent studies have demonstrated that regulating microglial and astrocytic hyperactivation can attenuate the inflammatory response. Therefore, targeting glial cells during SAE holds significant therapeutic potential, offering a promising avenue for the development of new strategies aimed at reversing the exacerbated CNS inflammatory response, mitigating neuronal damage, and ultimately reducing the long-term neurological sequelae observed in post-septic patients.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"89-100"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13004613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146086575","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":"Depressive Symptoms in Obese Individuals Accompanied by Greater Basal Inflammation but Lower Monocyte Inflammatory Responses to LPS: A Quest to Uncover Immunologic Links between Depression and Obesity.","authors":"Suzi Hong, Jordan Kohn, Stoyan Dimitrov, Christopher S Pruitt, Tiefu Cheng, Farah Shaikh","doi":"10.1159/000552352","DOIUrl":"10.1159/000552352","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Despite the high prevalence of co-occurring conditions between obesity and depression, the knowledge of the underlying mechanisms remains limited. Given the existing evidence of obesity being an inflammatory condition and the association between elevated inflammation and treatment-resistant depression, investigations to uncover immune pathways underlying the obesity-depression link will shed light on the mechanisms and therapeutic options. We investigated whether depressive symptoms and adiposity are associated with greater inflammation and with suppressed innate immune responses to an immune challenge.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Immune activities and depressive symptoms using the Beck Depression Inventory (BDI) were assessed in 96 participants of a weight range (normal weight, overweight, or obesity). Percent adiposity was measured by dual-energy X-ray absorptiometry. Plasma C-reactive protein (CRP), tumor necrosis factor (TNF), interleukin (IL)-1β, and IL-6 levels were determined by immunoassay. Lipopolysaccharides (LPSs)-stimulated intracellular TNF in peripheral blood monocytes was assessed by flow cytometry, which was also examined after incubation with recombinant TNF (rTNF) in 10 healthy participants of normal body mass index (BMI).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Obese, but not overweight, participants showed significantly higher BDI scores (T&lt;sub&gt;93&lt;/sub&gt; = 2.70, p &lt; 0.05) and plasma levels of CRP (T&lt;sub&gt;95&lt;/sub&gt; = 3.71, p &lt; 0.01), but lower LPS-stimulated monocytic TNF production (T&lt;sub&gt;93&lt;/sub&gt; = 3.23, p &lt; 0.01), than normal-weight subjects. Depressive symptoms were associated with BMI, % total and trunk fat, and plasma CRP levels (rs 0.22-0.35) but not with monocytic TNF production in univariate model. The association between BDI and inflammatory markers largely diminished after adjusting for demographic variables and blood pressure, and the association with obesity/adiposity disappeared in the final multivariate model. Plasma TNF levels and monocytic TNF production were negatively associated (r = -0.37, p &lt; 0.05) in univariate but not in multivariate models after controlling for covariates. BMI (β&lt;sub&gt;std&lt;/sub&gt; = -0.33), %total fat (β&lt;sub&gt;std&lt;/sub&gt; = -0.54), and %trunk fat (β&lt;sub&gt;std&lt;/sub&gt; = -0.57) remained significant predictors for monocyte TNF production even after controlling for demographic and plasma inflammatory marker levels (all ps &lt; 0.01). Prolonged (24-h) exposure of blood monocytes to rTNF in vitro suppressed LPS-stimulated monocytic TNF production in a dose-dependent manner, whereas acute rTNF pre-treatment potentiated TNF production.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Our findings provide the evidence that greater adiposity is associated with depressive symptoms and that obese individuals even without clinical depression experience elevated depressive symptoms. Whether immunologic dysregulation underlies this depressive mood-adiposity association is inconclusive despite greater CRP","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"264-277"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13348235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147840762","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":"Neuroinflammatory Aspects of Early Life Malnutrition and the Impacts on the Refinement of Neural Circuitry and Plasticity.","authors":"Claudio A Serfaty, Patricia Coelho de Velasco, Mariana Pereira de Freitas, Julia Huber Ferreira, Luana da Silva Chagas","doi":"10.1159/000551790","DOIUrl":"10.1159/000551790","url":null,"abstract":"<p><strong>Background: </strong>Communication between the nervous and immune systems plays a critical role during brain development. Under physiological conditions, microglia and astrocytes act as major players in developmental processes, such as neurogenesis, axon outgrowth, synaptic formation, pruning, myelination, and neural plasticity.</p><p><strong>Summary: </strong>However, chronic or excessive immune activation contributes to glial dysfunction and major disruption of synaptic pruning and adjustment of developing neural circuitry. Thus, inflammatory insults such as maternal infection, metabolic stress, or malnutrition such as lack essential nutrients (omega-3 fatty acids or tryptophan) or an excess of saturated fat and/or ultra-processed foods, alter inflammatory markers leading to abnormal microglial/astrocytic activation.</p><p><strong>Key messages: </strong>Together, those findings underscore the dual nature of neuroinflammation as both a regulator of normal development and a driver of abnormal development when dysregulated. Understanding how neural, immune and metabolic cues converge to influence glial and neuronal function is essential for developing strategies to prevent or mitigate the long-term consequences of early life malnutrition on successful brain development during critical periods of postnatal life.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"173-179"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147574930","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":"The Forgotten Beats.","authors":"Andrei P Sommer","doi":"10.1159/nim/adxag001","DOIUrl":"10.1159/nim/adxag001","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"349-354"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075275","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":"Some Basics on Innate Neuroimmunology for Nonspecialists.","authors":"Jan Pieter Konsman","doi":"10.1159/000550200","DOIUrl":"10.1159/000550200","url":null,"abstract":"<p><strong>Background: </strong>Although this seems to be common knowledge among experts, it is important to remind readers that two populations, namely, brain microglia and macrophages, found in different compartments of the central nervous system, play essential roles in innate neuroimmunology.</p><p><strong>Summary: </strong>Here, some historical and conceptual background will be provided that should allow the reader to place recent findings on these cells in some context and perspective.</p><p><strong>Key messages: </strong>It will be argued that (1) the brain is not devoid of immune response, but does represent an immune-privileged site, (2) innate neuroimmunology concerns brain border macrophages and parenchymal microglia, (3) even though brain border macrophages have been less extensively studied than parenchymal microglia, it is progressively becoming clear that these populations play different roles in physiological and pathological conditions and (4) while it is tempting to only use the latest technologies to obtain new findings, it is also essential, for the sake of science, to \"triangulate\" with findings obtained with more classic approaches. To determine whether and when innate neuroimmune responses are protective or pathological will be an important aim for future research.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"7-18"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878712","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":"Glucocorticoids and Neutrophil Biology: Impact on the Development of Resistance to Glucocorticoid Therapy.","authors":"Fabiana Santos Pacheco, Rayssa Garcia da Rocha Mota, Yago Amigo Pinho Jannini de Sá, Cory M Hogaboam, Hugo Caire Castro-Faria-Neto, Vinicius Frias Carvalho","doi":"10.1159/000551742","DOIUrl":"10.1159/000551742","url":null,"abstract":"<p><strong>Background: </strong>Neutrophils are the most abundant leukocytes in peripheral circulation and play a crucial role in combating infections and mediating inflammatory responses. Neutrophils are produced in bone marrow, have a short half-life in the blood, and are rapidly attracted to the tissues in response to infection or tissue damage.</p><p><strong>Summary: </strong>Glucocorticoids (GCs), stress hormones, and potent anti-inflammatory agents exert complex effects on neutrophils. While they generally suppress immune responses, GCs can paradoxically enhance neutrophil survival and function under certain conditions. This duality is evident in their ability to delay neutrophil apoptosis and to induce a shift of neutrophils from the marginated to the circulating pool, increasing the neutrophil presence in the bloodstream. Th17 cells, a subset of T-helper cells, recruit neutrophils to sites of infection and inflammation. In addition, neutrophils promote Th17 cell differentiation. GCs can enhance Th17 differentiation and IL-17 production, exacerbating neutrophil accumulation. Nevertheless, in glucocorticoid-resistant diseases, including multiple sclerosis (MS), traumatic brain injury (TBI), and encephalomyelitis, Th17 cells and neutrophils contribute to persistent inflammation. This resistance complicates the treatment of autoimmune diseases and chronic inflammatory disorders, also in the central nervous system, where standard glucocorticoid therapy fails to mitigate symptoms effectively.</p><p><strong>Key messages: </strong>In this context, we propose a mechanism for the development of resistance to GC driving by uncontrolled TH17 response and neutrophils induced by chronic stress. Understanding the interactions between neutrophils, Th17 cells, and GCs is essential for developing targeted therapies for diseases resistant to GC, such as MS, TBI, and encephalomyelitis.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"213-224"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262998/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593454","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":"In vivo Effects of Acute Inflammatory Responses on Dopaminergic Receptor Expression in Leukocytes and Marginal Effects of Hypoxia Pretreatment.","authors":"Leonie Fleige, Marie Jakobs, Gina Brüggemann, Bastian Tebbe, Tina Martin Schäper, Harald Engler, Anna Lena Friedel, Tina Hörbelt-Grünheidt, Joachim Fandrey, Manfred Schedlowski, Silvia Capellino","doi":"10.1159/000550768","DOIUrl":"10.1159/000550768","url":null,"abstract":"<p><strong>Introduction: </strong>Lipopolysaccharide (LPS) is widely used to study the mechanisms underlying acute inflammation. Interestingly, several studies suggest that LPS also regulates central dopaminergic signaling. Despite these findings in the brain, the effects of LPS on the dopaminergic system in the periphery remain poorly understood. Notably, peripheral immune cells express dopamine receptors (DRs) and can respond to dopamine. Dysregulation of the dopaminergic system in immune cells has been reported in various chronic inflammatory conditions. Additionally, studies suggest that hypoxia may also modulate dopamine synthesis and potentially amplify LPS-induced effects.</p><p><strong>Methods: </strong>The aim of this study was to investigate the effects of peripheral LPS administration on the dopaminergic system in male human peripheral blood mononuclear cells by measuring dopamine plasma levels and the expression of tyrosine hydroxylase and DRs. Additionally, we explored whether these effects are modulated by prior hypoxic exposure.</p><p><strong>Results: </strong>Our results suggest that in vivo LPS modulates the expression of DRs on monocytes and natural killer cells, as reflected by an upregulation after 24 h. In contrast, the effects of LPS on T and B cells were weaker, with a predominantly inhibitory influence on DR expression, supporting the notion of a cell-specific effect of LPS on dopaminergic signaling within the immune system. Additionally, our results indicate that hypoxic pretreatment did not alter LPS-induced changes in the dopaminergic pathway.</p><p><strong>Conclusion: </strong>Taken together, this study demonstrates for the first time that systemic LPS administration modulates DR expression in male peripheral immune cells. Further, our in vitro findings suggest that it is the LPS-induced immune response, rather than LPS itself, that drives changes in the dopaminergic pathway in specific immune cell subpopulations. However, further research is needed to elucidate the functional relevance of these findings in clinical contexts.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"138-149"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13078749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369891","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}