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肠道高毒力菌株通过下调色氨酸-吲哚丙酸-白细胞介素22轴诱导肝脓肿。

Liver abscess induced by intestinal hypervirulent through down-regulation of tryptophan-IPA-IL22 axis.

作者信息

You Xiu, Wang Liping, Wang Hong, Xu Yizheng, Chen Yongzheng, Xu Huizhen, Ji Xuelian, Ma Xiangsong, Xu Xiuyu

机构信息

Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Key Laboratory of Laboratory Medical Designated by the Ministry of Education, School of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, China.

出版信息

iScience. 2024 Aug 30;27(10):110849. doi: 10.1016/j.isci.2024.110849. eCollection 2024 Oct 18.

DOI:10.1016/j.isci.2024.110849
PMID:39429788
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11490733/
Abstract

Hypervirulent (hvKp) is a significant causative agent of invasive hepatic abscess syndrome in Asia, presenting substantial clinical challenges due to its intricate pathogenesis. This study revealed the crucial role of the gut microbiota in fortifying the host's defense against hvKp infection by enhancing interleukin-22 (IL-22), probably through regulating downstream antimicrobial peptides such as Reg3β. In antibiotic-treated mice, we observed that gut microbiota disruption impaired the transformation of tryptophan to indole, a key ligand for the aryl hydrocarbon receptor (AhR), consequently affecting the regulatory functions of IL-22. Our experimental findings revealed that administering rIL-22 or indole propionic acid notably diminished the translocation of hvKp from the intestine to the liver. This research not only underscores the pivotal role of the gut microbiome in modulating tryptophan metabolism and the IL-22 pathway but also highlights its critical function in preventing hvKp migration from the colon to the liver.

摘要

高毒力肺炎克雷伯菌（hvKp）是亚洲侵袭性肝脓肿综合征的重要病原体，因其复杂的发病机制带来了重大临床挑战。本研究揭示了肠道微生物群通过增强白细胞介素-22（IL-22），可能是通过调节下游抗菌肽如Reg3β，在加强宿主对hvKp感染的防御中发挥的关键作用。在抗生素处理的小鼠中，我们观察到肠道微生物群的破坏会损害色氨酸向吲哚的转化，吲哚是芳烃受体（AhR）的关键配体，从而影响IL-22的调节功能。我们的实验结果表明，给予重组IL-22或吲哚丙酸可显著减少hvKp从肠道向肝脏的移位。这项研究不仅强调了肠道微生物群在调节色氨酸代谢和IL-22途径中的关键作用，还突出了其在防止hvKp从结肠迁移到肝脏中的关键功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/db324e0f503e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/e7809abaed7f/fx1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/81cb6db26516/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/e0d745e24ebf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/6572b18e5cd2/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/432c321801d2/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/db324e0f503e/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/e7809abaed7f/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/73aef63dc2f9/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/6b5c5fc39dcf/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/81cb6db26516/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/e0d745e24ebf/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/6572b18e5cd2/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/432c321801d2/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd97/11490733/db324e0f503e/gr7.jpg

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本文引用的文献

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IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis.白介素-22 通过激活自噬促进闭合蛋白的表达，从而治疗溃疡性结肠炎。
Mol Cell Biochem. 2024 Jun;479(6):1443-1450. doi: 10.1007/s11010-023-04806-z. Epub 2023 Jul 13.
2
Gas6 ameliorates intestinal mucosal immunosenescence to prevent the translocation of a gut pathobiont, Klebsiella pneumoniae, to the liver.Gas6 可改善肠道黏膜免疫衰老，防止肠道共生菌肺炎克雷伯菌向肝脏易位。
PLoS Pathog. 2023 Jun 8;19(6):e1011139. doi: 10.1371/journal.ppat.1011139. eCollection 2023 Jun.
3
The Type VI Secretion System Contributes to the Invasiveness of Liver Abscess Caused by Klebsiella pneumoniae.
VI型分泌系统有助于肺炎克雷伯菌引起的肝脓肿的侵袭性。
J Infect Dis. 2023 Oct 18;228(8):1127-1136. doi: 10.1093/infdis/jiad166.
4
Hypercapsule is the cornerstone of in inducing pyogenic liver abscess.经皮穿刺引流术是治疗化脓性肝脓肿的基石。
Front Cell Infect Microbiol. 2023 Mar 31;13:1147855. doi: 10.3389/fcimb.2023.1147855. eCollection 2023.
5
Differences in severity of bacteraemia caused by hypermucoviscous and non-hypermucoviscous Klebsiella pneumoniae.产超黏液与非产超黏液肺炎克雷伯菌引起菌血症严重程度的差异。
Int J Antimicrob Agents. 2023 May;61(5):106767. doi: 10.1016/j.ijantimicag.2023.106767. Epub 2023 Feb 28.
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Cross-protection and cross-feeding between Klebsiella pneumoniae and Acinetobacter baumannii promotes their co-existence.肺炎克雷伯菌和鲍曼不动杆菌之间的交叉保护和交叉喂养促进了它们的共存。
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