Department of Oral Microbiology, Division of Oral Infection Health Sciences, Asahi University School of Dentistry, 1851 Hozumi, Mizuho, Gifu 501-0296, Japan.
J Med Microbiol. 2021 Mar;70(3). doi: 10.1099/jmm.0.001303. Epub 2021 Jan 13.
Food allergies (FAs) occur due to intestinal immune dysfunction elicited by dysbiotic conditions. It was previously determined by us that species propagate in the faeces of mice with FAs and worsen allergic symptoms by inducing the allergenic cytokine IL-33. Dendritic cells can play important roles in regulation of FA responses. species propagating in intestines of mice worsen allergic symptoms by stimulating dendritic cells to induce IL-33 expression. The aim of the present study was to analyse whether stimulates dendritic cells to induce IL-33 expression. IL-33 expression was evaluated in a DC2.4 mouse dendritic cell line stimulated by live or heat-inactivated JCM1658, ATP, LPS extracted from JCM1658 or other enterobacteria by real-time PCR. The ATP concentration and number of live bacteria in the culture supernatant were measured simultaneously. Live JCM1658 induced higher levels of IL-33 expression than other enterobacteria tested, but such a response was not elicited by heat-inactivated JCM1658. LPS extracted from JCM1658 did not induce IL-33 expression and suppressed live JCM1658-induced IL-33 expression via the activation of Toll-like receptor 4 signalling. Furthermore, ATP produced by JCM1658 stimulated dendritic cells to induce IL-33 expression by stimulating the P2X receptor, and LPS attenuated extracellular ATP-induced IL-33 expression. JCM1658 was observed to proliferate more vigorously and produce more ATP than other enterobacteria. acts as an allergenic bacterium through ATP production, stimulating dendritic cells to induce IL-33 expression, while LPS released from inactivated JCM1658 attenuates this allergenicity.
食物过敏(FA)是由于肠道免疫功能障碍引起的。我们之前已经确定, 物种在 FA 小鼠的粪便中繁殖,并通过诱导过敏细胞因子 IL-33 加重过敏症状。树突状细胞在调节 FA 反应中可以发挥重要作用。在肠道中繁殖的 物种通过刺激树突状细胞诱导 IL-33 表达来加重过敏症状。本研究的目的是分析 是否刺激树突状细胞诱导 IL-33 表达。通过实时 PCR 评估活的或热灭活的 JCM1658、来自 JCM1658 或其他肠杆菌的 ATP、LPS 刺激 DC2.4 小鼠树突状细胞系后 IL-33 的表达。同时测量培养上清液中 ATP 浓度和活细菌数量。与测试的其他肠杆菌相比,活的 JCM1658 诱导更高水平的 IL-33 表达,但热灭活的 JCM1658 不会引起这种反应。从 JCM1658 提取的 LPS 不会诱导 IL-33 表达,并且通过激活 Toll 样受体 4 信号通路抑制活的 JCM1658 诱导的 IL-33 表达。此外,JCM1658 产生的 ATP 通过刺激 P2X 受体刺激树突状细胞诱导 IL-33 表达,而 LPS 减弱细胞外 ATP 诱导的 IL-33 表达。与其他肠杆菌相比,JCM1658 观察到更旺盛的增殖和产生更多的 ATP。 通过产生 ATP 刺激树突状细胞诱导 IL-33 表达,从而成为一种变应原菌,而从失活的 JCM1658 释放的 LPS 减轻了这种变应原性。