由清酒乳杆菌衍生的膜泡增强派尔集合淋巴结细胞 IgA 产生的机制。
Mechanisms underlying enhanced IgA production in Peyer's patch cells by membrane vesicles derived from Lactobacillus sakei.
机构信息
Chemistry, Materials and Bioengineering Major, Graduate School of Science and Engineering, Kansai University, Suita, Osaka, Japan.
Laboratory of Vaccine Materials, Center for Vaccine and Adjuvant Research and Laboratory of Gut Environmental System, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
出版信息
Biosci Biotechnol Biochem. 2021 May 25;85(6):1536-1545. doi: 10.1093/bbb/zbab065.
We analyzed the mechanisms underlying enhanced IgA production in the cells of Peyer's patch cells via membrane vesicles derived from Lactobacillus sakei subsp. sakei NBRC 15893. Depletion of CD11c+ cells from Peyer's patch cells suppressed the enhanced IgA production mediated by membrane vesicles. Meanwhile, the stimulation of bone-marrow-derived dendritic cells with membrane vesicles increased gene expression of inducible nitric oxide synthase, retinaldehyde dehydrogenase 2, and several inflammatory cytokines. The production of nitric oxide and interleukin (IL)-6 by membrane vesicle stimulation was induced via Toll-like receptor 2 on bone marrow-derived dendritic cells. Inhibition of inducible nitric oxide synthase and retinaldehyde dehydrogenase 2, as well as the neutralization of IL-6 in Peyer's patch cells, suppressed the enhanced IgA production by membrane vesicle stimulation. Hence, nitric oxide, retinoic acid, and IL-6 induced by membrane vesicles play crucial roles in the enhanced IgA production elicited by membrane vesicles in Peyer's patch cells.
我们分析了通过源自清酒乳杆菌亚种 sakei NBRC 15893 的膜泡增强派伊尔氏结细胞中 IgA 产生的机制。耗尽派伊尔氏结细胞中的 CD11c+细胞会抑制膜泡介导的增强的 IgA 产生。同时，用膜泡刺激骨髓来源的树突状细胞会增加诱导型一氧化氮合酶、视黄醛脱氢酶 2 和几种炎症细胞因子的基因表达。膜泡刺激诱导骨髓来源的树突状细胞上 Toll 样受体 2 产生一氧化氮和白细胞介素 (IL)-6。抑制诱导型一氧化氮合酶和视黄醛脱氢酶 2 ，以及中和派伊尔氏结细胞中的 IL-6 ，会抑制膜泡刺激引起的增强的 IgA 产生。因此，膜泡诱导的一氧化氮、视黄酸和 IL-6 在膜泡刺激派伊尔氏结细胞中引起的增强的 IgA 产生中发挥关键作用。
Zotero 插件