International Journal of Molecular Sciences · 9 authors, 5 centres
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Using a restraint stress mouse model, this preclinical study demonstrated that psychological stress induces immunosuppression through macrophage pyroptosis in the spleen, a mechanism distinct from the P-selectin-dependent immunosuppression caused by cold exposure or IVIg. Treatment with NLRP3 inflammasome inhibitors reversed restraint-stress-induced macrophage pyroptosis, IL-1β expression, and spleen infiltration.
Researchers used a restraint stress model in C57Bl/6J mice to investigate psychological-stress-induced immunosuppression, comparing it with cold exposure and IVIg treatments. Anxiety-like behaviors confirmed psychological stress involvement. Restraint stress elevated plasma corticosterone and cortisol levels and induced immunosuppression that was mechanistically distinct from the P-selectin-dependent pathway mediating cold exposure- and IVIg-induced immunosuppression. Restraint stress led to gastrointestinal leakage, increased leukocyte infiltration into the spleen, reduced phagocyte function, and macrophage cell death via pyroptosis. Notably, treatment with NLRP3 inflammasome inhibitors OLT1177 and Z-WEHD-FMK reversed macrophage pyroptosis, pro-inflammatory cytokine IL-1β expression, and spleen infiltration. Limitations include the inability to extrapolate findings to human immune disturbances and the incompletely elucidated mechanism underlying restraint-stress-induced immunosuppression. The findings suggest macrophage pyroptosis as a potential therapeutic target for stress-induced immunosuppression.
