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瞬时受体电位阳离子通道亚家族M成员8（TRPM8）和肾素-血管紧张素-醛固酮系统（RAAS）介导的高血压对小鼠冷诱导的免疫抑制至关重要。

TRPM8 and RAAS-mediated hypertension is critical for cold-induced immunosuppression in mice.

作者信息

Chan Hao, Huang Hsuan-Shun, Sun Der-Shan, Lee Chung-Jen, Lien Te-Sheng, Chang Hsin-Hou

机构信息

Institute of Medical Sciences, Tzu-Chi University, Hualien, Taiwan.

Center for Prevention and Therapy of Gynecological Cancers, Department of Research, Buddhist Tzu Chi General Hospital, Hualien, Taiwan.

出版信息

Oncotarget. 2018 Jan 30;9(16):12781-12795. doi: 10.18632/oncotarget.24356. eCollection 2018 Feb 27.

DOI:10.18632/oncotarget.24356
PMID:29560109
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5849173/
Abstract

Mechanisms underlying cold-induced immunosuppression remain unclear. Here we found that cold exposure leads to transient receptor potential melastatin 8 (TRPM8)-dependent, renin-angiotensin-aldosterone system (RAAS)-mediated hypertension, which subsequently induces small molecule and fluid extravasation, increases plasma Ig levels, and elicits immunosuppression. An effect is similar to the clinically-used immunosuppressive treatments of intravenous immunoglobulin (IVIg) against various inflammatory diseases, such as immune thrombocytopenia (ITP). Essential roles of TRPM8 and Ig in cold-induced immunosuppression are supported by the cold-mediated amelioration of ITP and the cold-mediated suppression of bacterial clearance, which were observed in wild-type mice but not in Ig- and TRPM8-deficient mutants. Treatment with antihypertensive drugs aliskiren and losartan drastically reversed high plasma Ig levels and ameliorated cold-induced immunosuppression, indicating the involvement of the RAAS and hypertension. These results indicated that the natively increased plasma Ig level is associated with immunosuppression during periods of cold exposure, and antihypertensive drugs can be useful to manage cold-induced immunosuppression.

摘要

寒冷诱导的免疫抑制背后的机制仍不清楚。在此，我们发现冷暴露会导致瞬时受体电位香草酸亚型8（TRPM8）依赖性、肾素-血管紧张素-醛固酮系统（RAAS）介导的高血压，进而诱导小分子和液体外渗，增加血浆免疫球蛋白（Ig）水平，并引发免疫抑制。这一效应类似于临床上用于治疗各种炎症性疾病（如免疫性血小板减少症（ITP））的静脉注射免疫球蛋白（IVIg）免疫抑制治疗。TRPM8和Ig在寒冷诱导的免疫抑制中的重要作用得到了以下证据的支持：在野生型小鼠中观察到寒冷介导的ITP改善和细菌清除抑制，但在Ig和TRPM8缺陷突变体中未观察到。使用抗高血压药物阿利吉仑和氯沙坦进行治疗可显著逆转高血浆Ig水平，并改善寒冷诱导的免疫抑制，表明RAAS和高血压参与其中。这些结果表明，在冷暴露期间，内源性升高的血浆Ig水平与免疫抑制有关，抗高血压药物可能有助于控制寒冷诱导的免疫抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/cce42355fc18/oncotarget-09-12781-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/9c95e6266fb9/oncotarget-09-12781-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/83b9ca8965de/oncotarget-09-12781-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/002b7aef62c9/oncotarget-09-12781-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/3a8f48d0b144/oncotarget-09-12781-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/d26574b77e2a/oncotarget-09-12781-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/e318f4d3993c/oncotarget-09-12781-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/cfa3eb8c7cf7/oncotarget-09-12781-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/1a0f9e73ecfe/oncotarget-09-12781-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/cce42355fc18/oncotarget-09-12781-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/9c95e6266fb9/oncotarget-09-12781-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/83b9ca8965de/oncotarget-09-12781-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/002b7aef62c9/oncotarget-09-12781-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/3a8f48d0b144/oncotarget-09-12781-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/d26574b77e2a/oncotarget-09-12781-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/e318f4d3993c/oncotarget-09-12781-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/cfa3eb8c7cf7/oncotarget-09-12781-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/1a0f9e73ecfe/oncotarget-09-12781-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18a8/5849173/cce42355fc18/oncotarget-09-12781-g009.jpg

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