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肠道菌群通过 NLRP3 在湿热环境中促进 Th2 介导的免疫。

Intestinal microflora promotes Th2-mediated immunity through NLRP3 in damp and heat environments.

机构信息

State Key Laboratory of Traditional Chinese Medicine Syndrome, Guangzhou University of Chinese Medicine, Guangzhou, China.

School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

Front Immunol. 2024 May 2;15:1367053. doi: 10.3389/fimmu.2024.1367053. eCollection 2024.

DOI:10.3389/fimmu.2024.1367053
PMID:38756775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11096527/
Abstract

BACKGROUND

With the worsening of the greenhouse effect, the correlation between the damp-heat environment (DH) and the incidence of various diseases has gained increasing attention. Previous studies have demonstrated that DH can lead to intestinal disorders, enteritis, and an up-regulation of NOD-like receptor protein 3 (NLRP3). However, the mechanism of NLRP3 in this process remains unclear.

METHODS

We established a DH animal model to observe the impact of a high temperature and humidity environment on the mice. We sequenced the 16S rRNA of mouse feces, and the RNA transcriptome of intestinal tissue, as well as the levels of cytokines including interferon (IFN)-γ and interleukin (IL)-4 in serum.

RESULTS

Our results indicate that the intestinal macrophage infiltration and the expression of inflammatory genes were increased in mice challenged with DH for 14 days, while the M2 macrophages were decreased in mice. The alpha diversity of intestinal bacteria in mice was significantly higher than that in control mice, including an up-regulation of the ratio. Transcriptomic analysis revealed 307 differentially expressed genes were decreased in mice compared with control mice, which was related to humoral immune response, complement activation, phagocytic recognition, malaria and inflammatory bowel disease. The ratio of IFN-γ/IL-4 was decreased in control mice but increased in mice.

CONCLUSIONS

Our study found that the inflammation induced by DH promotes Th2-mediated immunity via NLRP3, which is closely related to the disruption of intestinal flora.

摘要

背景

随着温室效应的恶化，湿热环境（DH）与各种疾病发病率之间的相关性受到越来越多的关注。先前的研究表明，DH 可导致肠道紊乱、肠炎和 NOD 样受体蛋白 3（NLRP3）的上调。然而，NLRP3 在这一过程中的机制尚不清楚。

方法

我们建立了 DH 动物模型来观察高温高湿环境对小鼠的影响。我们对小鼠粪便的 16S rRNA 进行测序，对肠道组织的 RNA 转录组以及血清中干扰素（IFN）-γ和白细胞介素（IL）-4 等细胞因子的水平进行检测。

结果

我们的结果表明，DH 刺激 14 天后，小鼠肠道巨噬细胞浸润和炎症基因表达增加，而 M2 巨噬细胞减少。DH 刺激小鼠的肠道细菌 alpha 多样性明显高于对照组，包括上调比。转录组分析显示，与对照组相比，DH 刺激小鼠有 307 个差异表达基因下调，这些基因与体液免疫反应、补体激活、吞噬识别、疟疾和炎症性肠病有关。IFN-γ/IL-4 的比值在对照组中降低，但在 DH 刺激小鼠中增加。

结论

本研究发现，DH 引起的炎症通过 NLRP3 促进 Th2 介导的免疫，这与肠道菌群的破坏密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/1fe3eb663237/fimmu-15-1367053-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/1a204cc9af69/fimmu-15-1367053-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/84a9e4228df7/fimmu-15-1367053-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/df6fcdb6b6d4/fimmu-15-1367053-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/40c690251c6c/fimmu-15-1367053-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/81fac349ec41/fimmu-15-1367053-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/1fe3eb663237/fimmu-15-1367053-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/1a204cc9af69/fimmu-15-1367053-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/84a9e4228df7/fimmu-15-1367053-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/df6fcdb6b6d4/fimmu-15-1367053-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/40c690251c6c/fimmu-15-1367053-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/81fac349ec41/fimmu-15-1367053-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc6a/11096527/1fe3eb663237/fimmu-15-1367053-g006.jpg

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