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束缚应激诱导的免疫抑制与小鼠中同时发生的巨噬细胞焦亡细胞死亡有关。

Restraint Stress-Induced Immunosuppression Is Associated with Concurrent Macrophage Pyroptosis Cell Death in Mice.

机构信息

Department of Hematology and Oncology, Buddhist Tzu Chi General Hospital, Hualien 970, Taiwan.

Center of Stem Cell & Precision Medicine, Hualien Tzu Chi Hospital, Hualien 970, Taiwan.

出版信息

Int J Mol Sci. 2023 Aug 17;24(16):12877. doi: 10.3390/ijms241612877.

DOI:10.3390/ijms241612877
PMID:37629059
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10454201/
Abstract

Psychological stress is widely acknowledged as a major contributor to immunosuppression, rendering individuals more susceptible to various diseases. The complex interplay between the nervous, endocrine, and immune systems underlies stress-induced immunosuppression. However, the underlying mechanisms of psychological-stress-induced immunosuppression remain unclear. In this study, we utilized a restraint stress mouse model known for its suitability in investigating physiological regulations during psychological stress. Comparing it with cold exposure, we observed markedly elevated levels of stress hormones corticosterone and cortisol in the plasma of mice subjected to restraint stress. Furthermore, restraint-stress-induced immunosuppression differed from the intravenous immunoglobulin-like immunosuppression observed in cold exposure, with restraint stress leading to increased macrophage cell death in the spleen. Suppression of pyroptosis through treatments of inflammasome inhibitors markedly ameliorated restraint-stress-induced spleen infiltration and pyroptosis cell death of macrophages in mice. These findings suggest that the macrophage pyroptosis associated with restraint stress may contribute to its immunosuppressive effects. These insights have implications for the development of treatments targeting stress-induced immunosuppression, emphasizing the need for further investigation into the underlying mechanisms.

摘要

心理压力被广泛认为是免疫抑制的主要因素,使个体更容易患上各种疾病。神经、内分泌和免疫系统之间的复杂相互作用是心理压力引起免疫抑制的基础。然而,心理压力引起免疫抑制的潜在机制尚不清楚。在这项研究中,我们使用了一种束缚应激小鼠模型,该模型适合研究心理应激过程中的生理调节。与冷暴露相比,我们观察到束缚应激小鼠血浆中的应激激素皮质酮和皮质醇水平显著升高。此外,束缚应激引起的免疫抑制与冷暴露引起的静脉注射免疫球蛋白样免疫抑制不同,束缚应激导致脾脏中巨噬细胞死亡增加。通过使用炎性小体抑制剂抑制细胞焦亡,显著改善了束缚应激诱导的小鼠脾脏浸润和巨噬细胞细胞焦亡死亡。这些发现表明,与束缚应激相关的巨噬细胞细胞焦亡可能与其免疫抑制作用有关。这些研究结果为针对应激引起的免疫抑制的治疗方法的发展提供了依据,强调需要进一步研究其潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ac5/10454201/1af82a922536/ijms-24-12877-g007.jpg
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