Associations of serum α-synuclein and 1,3-β-D-glucan levels with sleep architecture alterations in chronic insomnia disorder.

Systemic Inflammatory Markers Correlate with Chronic Kidney Disease-Associated Pruritus and Response to Treatment.

Neuromedin B and its receptor NMBR inhibit H9N2 infection.

The VIP-VIPR2 axis strengthens intestinal barrier integrity and antimicrobial immunity in Ctenopharyngodon idella.

Histamine plays a central role in CSU pathogenesis and may contribute to extracutaneous symptoms such as dysmenorrhea, but this relationship has not been fully examined. In this prospective, cross-sectional multicenter study, 425 female CSU patients and 370 age-matched controls were recruited from 19 UCARE centers in Türkiye. Dysmenorrhea prevalence and severity were assessed using a numerical scale and symptom scores. Histamine skin prick testing (SPT) was performed to evaluate histamine clearance capacity. Associations between dysmenorrhea, CSU phenotype, antihistamine use, and SPT kinetics were analyzed. The prevalence and severity of dysmenorrhea were comparable between CSU patients and controls (81.6% vs. 79.5%, p = 0.244). However, 95/418 (22.7%) of CSU patients reported increased menstrual pain following CSU onset, and 20/95 (21.1%) of these reported partial relief with antihistamines. CSU patients with worsened dysmenorrhea exhibited significantly shorter histamine SPT positivity durations than those without symptom change (35 vs. 45 min; p = 0.015). No correlation was observed between dysmenorrhea severity and total IgE, anti-TPO levels, or urticaria control/activity scores. A moderate negative correlation was found between UAS7 and elapsed time to histamine SPT negativity (r = -0.389, p < 0.001). Although overall prevalence and severity of dysmenorrhea were similar in CSU patients and healthy controls, about one in five patients with CSU experienced worsening menstrual pain after disease onset, and only a subset of these patients reported partial improvement with antihistamines. A distinct CSU subgroup with heightened menstrual pain may be characterized by altered histamine dynamics. Whether these patients may benefit from more intensive antihistamine treatment remains uncertain and requires confirmation in future studies; further studies should explore neuroimmune and hormonal mechanisms underlying this overlap.

According to the World Health Organization, pain remains one of the leading causes for seeking medical care. The modern understanding of pain is grounded in the biopsychosocial model, reflecting its complex and multidimensional nature. In patients with rheumatic diseases, chronic pain represents a multifactorial continuum that often integrates nociceptive, neuropathic, and nociplastic mechanisms. This review analyzes the role of central sensitization (CS) and fibromyalgia (FM) in sustaining chronic pain among patients with rheumatic diseases, summarizing evidence from recent systematic reviews and meta-analyses on the prevalence of FM across rheumatic disorders and its impact on disease activity indices and quality of life. Current therapeutic strategies aimed at modulating CS and FM are discussed, including non-pharmacological interventions, centrally acting pharmacotherapies, and the emerging potential of Janus kinase (JAK) inhibitors, which may modulate both inflammatory and neuroimmune mechanisms of pain.

The skin is a highly innervated and immunologically active barrier organ, where neuro-immune interactions critically shape both physiological homeostasis and disease progression. Growing evidence indicates that bidirectional crosstalk between the nervous and immune systems is not only central to the pathogenesis of allergic skin diseases but also represents an emerging frontier for therapeutic innovation. In this review, we systematically examine atopic dermatitis (AD), contact dermatitis (CD), and urticaria, integrating insights into peripheral pathways-mediated by sensory neurons, cytokine networks, and immune cells-and central mechanisms involving the hypothalamic-pituitary-adrenal axis and higher neural circuits. By contrasting shared and disease-specific neuro-immune signatures, we highlight how these mechanisms underlie distinct inflammatory phenotypes and clinical manifestations. We further evaluate current and investigational therapies, including biologics and small molecules that target neuro-immune signaling, and discuss their translational significance. Looking ahead, we identify unresolved questions and propose future directions aimed at leveraging neuro-immune mechanisms to advance precision diagnosis and personalized interventions in allergic skin diseases.

Chronic cancer pain results from the complex interaction of nociceptive, neuropathic, and neuroimmune mechanisms, which vary according to tumor type, location, stage, and treatment history. Recent advances in cancer neuroscience have reframed pain as a dynamic manifestation of reciprocal tumor–nerve–immune interactions, rather than a mere consequence of tissue damage. In this model, malignant, stromal, and immune cells remodel nociceptive circuits at peripheral and central levels. This narrative review, conducted in accordance with SANRA criteria, synthesizes current mechanistic insights into the neurobiology of cancer pain. At the peripheral level, tumor-derived mediators such as prostaglandins, cytokines, chemokines, glutamate, and endothelin-1 drive nociceptor sensitization via G-protein–coupled and tyrosine kinase pathways. In bone metastases, osteoclast-mediated resorption generates an acidic microenvironment that activates acid-sensing ion channels and transient receptor potential (TRP) channels, linking skeletal destruction with movement-evoked pain. Pathological nerve remodeling and perineural invasion further contribute to neuropathic components and adverse oncological outcomes. Treatment-induced syndromes, notably chemotherapy-induced peripheral neuropathy, result from axonal injury, mitochondrial dysfunction, and neuroinflammation. At the central level, persistent afferent input induces glial activation and chemokine signaling, amplifying synaptic transmission and promoting central sensitization. Emerging evidence also highlights epigenetic regulation, noncoding RNAs, and tumor–immune–neural crosstalk as potential therapeutic targets. Collectively, these findings position cancer pain as a disorder of aberrant tumor–nerve–immune signaling. Effective management requires precision strategies integrating mechanism-guided pharmacology, neuromodulation, and supportive care. This review emphasizes the need for translational research to bridge mechanistic discoveries with personalized, multimodal interventions in oncology.

Cutaneous immunity operates through a complex integration of structural, microbial, cellular, and neuroimmune mechanisms that collectively determine the skin’s ability to maintain homeostasis and respond to injury or inflammation. This review synthesizes contemporary evidence on epidermal barrier dysfunction, microbiome dysbiosis, antigen-presenting cell networks, tissue-resident memory T cells, and neuroimmune signaling to construct a comprehensive model explaining the pathophysiology of major inflammatory dermatoses, including atopic dermatitis, psoriasis, and allergic contact dermatitis. Key findings highlight barrier impairment as an initiating factor in immune activation, microbial imbalance—particularly Staphylococcus aureus overgrowth—as a powerful amplifier of inflammatory responses, and specialized immune circuits as central drivers of chronicity. Neuroimmune interactions, although less frequently explored, emerge as critical contributors to persistent pruritus and symptom exacerbation. The integration of these mechanisms provides a unified framework that enhances understanding of disease heterogeneity and supports the development of targeted, context-specific approaches relevant to diverse populations such as those in Mexico, Colombia, and Ecuador. This multidimensional perspective reaffirms the skin as a fully active immune organ and underscores the value of coordinated strategies that address structural integrity, microbial ecology, immune regulation, and neural pathways.

Sympathetic remodeling following myocardial infarction (MI) is a critical mechanism underlying the development of malignant arrhythmias and sudden cardiac death (SCD). The cardiac sympathetic nervous system functions as a multi-level regulatory network, integrating centers from the cerebral cortex (e.g., the insular lobe and anterior cingulate gyrus), subcortical structures (e.g., the paraventricular nucleus of the hypothalamus), and brainstem nuclei (e.g., the rostral ventrolateral medulla and nucleus of the solitary tract), down to the peripheral ganglia. Post-MI, this entire neural axis undergoes significant remodeling, which manifests as neuroinflammation in the central nervous system, alongside peripheral sympathetic nerve sprouting and heterogeneous hyperinnervation. This article provides a systematic review of the anatomical architecture of the cardiac sympathetic nerve and the regulatory mechanisms of sympathetic remodeling at various levels of the central nervous system after MI. It particularly focuses on key signaling pathways—including the TLR4/MyD88/NF-κB and P2X7R/NLRP3 inflammasome pathways, as well as GABAergic inhibition within the paraventricular nucleus—in addition to the peripheral remodeling mechanisms within the stellate ganglia. By synthesizing insights from these studies, this review offers a novel perspective for understanding the neuroimmune mechanisms of post-MI malignant arrhythmias and provides a theoretical foundation for elucidating the mechanisms of SCD in clinical practice.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder centered around social disorders and stereotyped behavior, with its global prevalence increasing year by year. Traditional behavior and medication interventions have limited effectiveness. In recent years, the progress of the microbiota gut brain (MGB) axis theory has provided new directions for the etiology research and clinical nursing of ASD. The imbalance of gut microbiota in children with ASD can exacerbate neuroinflammation through neuroimmune mechanisms, further affecting central nervous system development. The nursing intervention strategy based on MGB axis can improve gastrointestinal symptoms and behavioral abnormalities in children with ASD. However, microbial intervention still faces multiple challenges. This review systematically integrates the clinical application and mechanism exploration of MGB axis in ASD, and constructs a nursing practice framework based on the existing research results of MGB axis, providing multidimensional theoretical support and practical path for optimizing ASD clinical nursing strategies.

IL-2/IL-2Rβγ signaling in pruriceptors drives neuroimmune mechanisms of nivolumab-induced persistent itch

Parkinson’s disease (PD) and Alzheimer’s disease (AD) present with complex behavioral symptoms that can arise in the absence of overt structural brain damage. Recent evidence suggests that border-associated macrophages (BAMs) located at the brain’s interfaces regulate central nervous system function, yet the specific roles of distinct BAM subsets remain largely undefined. By reanalyzing single-nucleus RNA sequencing data from postmortem PD brains, we identified a BAM subset expressing CD169 that was significantly reduced in patients compared with controls. To examine their function, we employed CD169-DTR mice to selectively ablate CD169+ BAMs and evaluated behavioral and histological changes. Depletion of CD169+ BAMs induced tremors, abnormal hindlimb reflexes, and heightened anxiety-like behavior without dopaminergic neuron loss. Histological analysis revealed a pronounced reduction of mitral and tufted cells in the olfactory bulb, indicating disruption of olfactory-limbic circuitry. These findings demonstrate that CD169+ BAMs are critical for maintaining neural network stability and motor function, and that their loss can elicit PD-like phenotypes in the absence of classical dopaminergic neurodegeneration. This work establishes a novel mouse model linking brain-border immune cell dysfunction to Parkinsonian pathology and highlights a neuroimmune mechanism that may contribute to the onset of PD-like disorders.

Sepsis, a life-threatening condition caused by a dysregulated host response to infection, continues to be a major cause of mortality in critical care despite medical advancements. This study aimed to investigate the therapeutic effects and neuroimmune mechanisms of electroacupuncture (EA) at the Shenshu (BL23) acupoint combined with antibiotic therapy in sepsis management. A cecal ligation and puncture (CLP)-induced murine sepsis model was used to evaluate the combined therapy. The study employed enzyme-linked immunosorbent assays (ELISA) and histological analysis to assess systemic inflammation and intestinal damage. Three-dimensional immunolabeling of c-Fos neurons and chemogenetic modulation of hypothalamic paraventricular nucleus (PVN) neurons were performed to investigate neural mechanisms. Additionally, serum catecholamine levels were measured using ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). The combination of EA and antibiotics significantly improved survival rates and reduced sepsis-induced weight loss. The therapy lowered systemic levels of proinflammatory cytokines (TNF-α and IL-6) and mitigated intestinal inflammatory infiltration. EA at BL23 suppressed neuronal activation in the PVN by reducing c-Fos expression. Chemogenetic inhibition of corticotropin-releasing hormone (CRH) neurons replicated the anti-inflammatory effects of the therapy, while their activation diminished therapeutic benefits. Conversely, activation of oxytocin (OXT) neurons reproduced the anti-inflammatory effects, and their inhibition reversed these benefits. The combined therapy also elevated serum catecholamine levels, indicating sympathetic-mediated immunomodulation. This study demonstrates that EA at BL23 enhances antibiotic efficacy in sepsis by modulating PVN activity-suppressing CRH neurons and activating OXT neurons-leading to increased catecholamine secretion and systemic inflammation control. These findings reveal a novel neuroimmunological pathway for acupuncture's therapeutic role in sepsis, supporting its potential as a noninvasive adjunctive therapy in critical care.

Recently, large epidemiological studies described those antimicrobial vaccinations were protective against AD. Whether these vaccinations prevent the deposition of amyloidosis in the brain is highly relevant to identify novel protective neuroimmune mechanisms. Pfizer COVID-19 and Fluarix vaccine were selected for this study. PBS and LPS were used as controls. Vaccine and control materials were intramuscularly administered 5 times (monthly doses) starting at 90 days old in APP/PS1 mice. Same number of male and female subjects were used. Seven days after the last treatment, a contextual behavioral test was applied to assess working memory. Aβ burden and neuroinflammatory markers were measured in brain samples and serum using histological and biochemical methods. Mice treated with Pfizer and Fluarix vaccines showed improved cognitive performance compared with the control group (PBS). Importantly, mice treated with the Pfizer vaccine displayed reduced Aβ burden in hippocampus, lateral areas of the cortex, and the insular cortex compared with control subjects. On the contrary, animals treated with the Fluarix vaccine did not show significant differences. Analyses to measure peripheral and brain inflammation were also conducted. The stimulation of the peripheral immune system by antimicrobial immunizations could impact the brain in a positive manner. Importantly, the levels of Aβ pathology were reduced in mice treated with the Pfizer COVID-19 vaccine. Further research in this area may provide us with valuable information about amyloidogenic and non-amyloidogenic neuroimmune mechanisms associated with AD.

Over-excitation of tyrosine hydroxylase neurons in the paraventricular nucleus of the hypothalamus drives a neuroimmune positive feedback loop in rheumatoid arthritis.

Regulatory T cells attenuate astrogliosis via IL-10/STAT3/PKC/vimentin signaling and promote neurological recovery after spinal cord injury.

Neuroimmune Mechanisms Transforming Acute Injury to Long-Term Brain Dysfunction After Sepsis

The evolution of food protein-induced enterocolitis syndrome (FPIES): Global trends, emerging triggers, and natural history.

An expert narrative review on the brain-kidney axis in diabetic kidney disease: Mechanisms and therapeutic insights.