BioAcyl Corp
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Zhang, Y.-S., Chen, H.-C., & Cao, J.-X. (2025). Oxytocin-mediate modulation of splenic immunosuppression in chronic social stress through neuroendocrine pathways. Advanced Science, n/a(n/a), 2500849. Added by: Dr. Enrique Feoli (23/06/2025, 21:50) Last edited by: Dr. Enrique Feoli (23/06/2025, 22:03) |
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| Resource type: Journal Article DOI: 10.1002/advs.202500849 BibTeX citation key: Zhang2025 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Oxytocin analgesia Keywords: brain-spleen interaction, chronic social stress, immune regulation, macrophage polarization, oxytocin Creators: Cao, Chen, Zhang Publisher: Wiley Collection: Advanced Science |
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| Abstract |
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Abstract Chronic social stress (CSS) is a significant public health challenge that negatively impacts behavior and immune function through brain-spleen interactions. Oxytocin (OT), a neuropeptide critical for social behavior and immune regulation, is upregulated during CSS, though its underlying mechanisms remain unclear. This study investigates the role of OT in splenic immune modulation using a murine model of CSS. Behavioral evaluations, serum oxytocin quantification, and splenic immunophenotypic analysis were performed. Splenic denervation confirmed OT’s neuromodulatory role, whereas OTR antagonism revealed its endocrine function. CSS-induced OT elevation was associated with immunosuppression, characterized by increased Foxp3⁺ regulatory T cells and reduced CD4⁺ T and CD19⁺ B cells. OT also modulated macrophage polarization, inhibiting M1-like (pro-inflammatory) and enhancing M2-like (anti-inflammatory) phenotypes. Denervation or pharmacological blockade of OT signaling partly reversed CSS-induced splenic immunosuppression but adversely affected survival in CSS-exposed mice. Additionally, denervation or OTR antagonism reduced the mice's response to social defeat, as shown by decreased social avoidance behavior. These findings suggest that OT-mediated immunosuppression likely represents a compensatory mechanism in response to chronic social stress. Targeting the OT–immune axis could offer innovative therapeutic approaches for stress-associated disorders by restoring immune homeostasis while maintaining behavioral integrity.
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