Suppr超能文献

通过增加小鼠派尔集合淋巴结中B细胞内活化诱导的胞苷脱氨酶表达,拟杆菌比乳酸杆菌诱导产生更高水平的IgA。

Bacteroides induce higher IgA production than Lactobacillus by increasing activation-induced cytidine deaminase expression in B cells in murine Peyer's patches.

作者信息

Yanagibashi Tsutomu, Hosono Akira, Oyama Akihito, Tsuda Masato, Hachimura Satoshi, Takahashi Yoshimasa, Itoh Kikuji, Hirayama Kazuhiro, Takahashi Kyoko, Kaminogawa Shuichi

机构信息

Department of Food Science and Technology, Nihon University, Fujisawa-shi, Kanagawa, Japan.

出版信息

Biosci Biotechnol Biochem. 2009 Feb;73(2):372-7. doi: 10.1271/bbb.80612. Epub 2009 Feb 7.

Abstract

The gut mucosal immune system is crucial in host defense against infection by pathogenic microbacteria and viruses via the production of IgA. Previous studies have shown that intestinal commensal bacteria enhance mucosal IgA production. However, it is poorly understood how these bacteria induce IgA production and which genera of intestinal commensal bacteria induce IgA production effectively. In this study, we compared the immunomodulatory effects of Bacteroides and Lactobacillus on IgA production by Peyer's patches lymphocytes. IgA production by Peyer's patches lymphocytes co-cultured with Bacteroides was higher than with Lactobacillus. In addition, the expression of activation-induced cytidine deaminase increased in co-culture with Bacteroides but not with Lactobacillus. We found that intestinal commensal bacteria elicited IgA production. In particular, Bacteroides induced the differentiation of Peyer's patches B cell into IgA(+) B cells by increasing activation-induced cytidine deaminase expression.

摘要

肠道黏膜免疫系统在宿主抵御致病性微生物和病毒感染方面起着关键作用,它通过产生IgA来实现这一功能。先前的研究表明,肠道共生细菌可增强黏膜IgA的产生。然而,目前对于这些细菌如何诱导IgA产生以及哪些肠道共生细菌属能有效诱导IgA产生,我们了解得还很少。在本研究中,我们比较了拟杆菌属和乳杆菌属对派尔集合淋巴结淋巴细胞产生IgA的免疫调节作用。与拟杆菌属共同培养的派尔集合淋巴结淋巴细胞产生的IgA高于与乳杆菌属共同培养的情况。此外,与拟杆菌属共同培养时,活化诱导胞嘧啶脱氨酶的表达增加,而与乳杆菌属共同培养时则没有增加。我们发现肠道共生细菌能引发IgA的产生。特别是,拟杆菌属通过增加活化诱导胞嘧啶脱氨酶的表达,诱导派尔集合淋巴结B细胞分化为IgA(+) B细胞。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验