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细菌易位通过调节大鼠 CD4 T 细胞加重 CCl 诱导的肝纤维化。

Bacterial translocation aggravates CCl-induced liver cirrhosis by regulating CD4 T cells in rats.

机构信息

The Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University, Hangzhou, Zhejiang 310003, China.

The State Key Laboratory for Diagnosis and Treatment of Infectious Disease, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, China.

出版信息

Sci Rep. 2017 Jan 30;7:40516. doi: 10.1038/srep40516.

DOI:10.1038/srep40516
PMID:28134306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5278361/
Abstract

Bacterial translocation (BT) is thought to play an important role in the development of liver cirrhosis, but the mechanisms have not been fully explored. This study aims to investigate the distribution of Treg (CD3CD4CD25Foxp3), Th17 (CD3CD4IL-17), and Th1 (CD3CD4IFN-γ) cells in the intestinal lamina propria, liver and blood and to explore their relationships with BT. Cirrhotic rats with ascites were induced by CCl. We found that there were lower levels of total protein and albumin, lower albumin/globulin ratio, lower body weight and higher spleen weight and ascites volume in cirrhotic rats with than without BT. We found that BT may cause increase of Treg cells in the proximal small intestine and decrease of Th17 cells in the whole intestine and blood in cirrhotic rats. It may also aggravate the CCl-induced decrease in Th1 cells in the whole intestine, liver, caecum, and blood and the CCl-induced increase in Th17 cells in the liver and Tregs in the distal small intestine, colon, and liver. Our data suggest that BT may aggravate liver injury and decrease liver function via an interaction with CD4 T Cells. The results of this study may be helpful for the development of new treatments for liver cirrhosis.

摘要

细菌易位(BT)被认为在肝硬化的发展中起重要作用,但机制尚未完全阐明。本研究旨在研究 Treg(CD3CD4CD25Foxp3)、Th17(CD3CD4IL-17)和 Th1(CD3CD4IFN-γ)细胞在肠固有层、肝脏和血液中的分布,并探讨它们与 BT 的关系。通过 CCl 诱导腹水肝硬化大鼠。我们发现,有 BT 的肝硬化大鼠的总蛋白和白蛋白水平较低,白蛋白/球蛋白比值较低,体重较低,脾重和腹水体积较高。我们发现,BT 可能导致肝硬化大鼠近端小肠 Treg 细胞增加,全肠和血液 Th17 细胞减少。它还可能加重 CCl 诱导的全肠、肝脏、盲肠和血液中 Th1 细胞减少,以及 CCl 诱导的肝脏中 Th17 细胞和远端小肠、结肠和肝脏中 Tregs 细胞增加。我们的数据表明,BT 可能通过与 CD4 T 细胞相互作用加重肝损伤和降低肝功能。本研究结果可能有助于开发肝硬化的新治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/9de79f711592/srep40516-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/7830bba946d5/srep40516-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/551a570d047c/srep40516-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/5abf6c39b782/srep40516-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/d97d3bdb4aff/srep40516-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/9de79f711592/srep40516-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/7830bba946d5/srep40516-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/551a570d047c/srep40516-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/5abf6c39b782/srep40516-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/d97d3bdb4aff/srep40516-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c573/5278361/9de79f711592/srep40516-f5.jpg

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