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前列腺素E通过抑制微生物群依赖性调节性T细胞促进肠道炎症。

Prostaglandin E promotes intestinal inflammation via inhibiting microbiota-dependent regulatory T cells.

作者信息

Crittenden Siobhan, Goepp Marie, Pollock Jolinda, Robb Calum T, Smyth Danielle J, Zhou You, Andrews Robert, Tyrrell Victoria, Gkikas Konstantinos, Adima Alexander, O'Connor Richard A, Davies Luke, Li Xue-Feng, Yao Hatti X, Ho Gwo-Tzer, Zheng Xiaozhong, Mair Amil, Vermeren Sonja, Qian Bin-Zhi, Mole Damian J, Gerasimidis Konstantinos, Schwarze Jürgen K J, Breyer Richard M, Arends Mark J, O'Donnell Valerie B, Iredale John P, Anderton Stephen M, Narumiya Shuh, Maizels Rick M, Rossi Adriano G, Howie Sarah E, Yao Chengcan

机构信息

Centre for Inflammation Research, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK.

SRUC Veterinary Services, Scotland's Rural College, Easter Bush Estate EH26 0PZ, UK.

出版信息

Sci Adv. 2021 Feb 12;7(7). doi: 10.1126/sciadv.abd7954. Print 2021 Feb.

DOI:10.1126/sciadv.abd7954
PMID:33579710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7880593/
Abstract

The gut microbiota fundamentally regulates intestinal homeostasis and disease partially through mechanisms that involve modulation of regulatory T cells (T), yet how the microbiota-T cross-talk is physiologically controlled is incompletely defined. Here, we report that prostaglandin E (PGE), a well-known mediator of inflammation, inhibits mucosal T in a manner depending on the gut microbiota. PGE through its receptor EP4 diminishes T-favorable commensal microbiota. Transfer of the gut microbiota that was modified by PGE-EP4 signaling modulates mucosal T responses and exacerbates intestinal inflammation. Mechanistically, PGE-modified microbiota regulates intestinal mononuclear phagocytes and type I interferon signaling. Depletion of mononuclear phagocytes or deficiency of type I interferon receptor diminishes PGE-dependent T inhibition. Together, our findings provide emergent evidence that PGE-mediated disruption of microbiota-T communication fosters intestinal inflammation.

摘要

肠道微生物群通过涉及调节性T细胞（T细胞）调节的机制，从根本上调节肠道稳态和疾病，但微生物群与T细胞之间的相互作用在生理上是如何受到控制的，目前尚未完全明确。在此，我们报告前列腺素E（PGE），一种著名的炎症介质，以依赖肠道微生物群的方式抑制黏膜T细胞。PGE通过其受体EP4减少对T细胞有利的共生微生物群。经PGE-EP4信号修饰的肠道微生物群的转移调节黏膜T细胞反应并加剧肠道炎症。从机制上讲，PGE修饰的微生物群调节肠道单核吞噬细胞和I型干扰素信号传导。单核吞噬细胞的耗竭或I型干扰素受体的缺乏会减弱PGE依赖性T细胞抑制。总之，我们的研究结果提供了新的证据，表明PGE介导的微生物群与T细胞通讯的破坏会促进肠道炎症。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/73bd34042a6d/abd7954-F7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/35e57bf7980a/abd7954-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/228a7d5d1bdf/abd7954-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/c9e55420005b/abd7954-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/4e2d26418cad/abd7954-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/7875a217e6eb/abd7954-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/0540974460c2/abd7954-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/73bd34042a6d/abd7954-F7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/35e57bf7980a/abd7954-F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/228a7d5d1bdf/abd7954-F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/c9e55420005b/abd7954-F3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/4e2d26418cad/abd7954-F4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/7875a217e6eb/abd7954-F5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/0540974460c2/abd7954-F6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84e3/7880593/73bd34042a6d/abd7954-F7.jpg

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本文引用的文献

[1]
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Eur J Immunol. 2020-2-27

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