Pivotal Advance: Bifidobacteria and Gram-negative bacteria differentially influence immune responses in the proinflammatory milieu of celiac disease
Pivotal Advance: Bifidobacteria and Gram-negative bacteria differentially influence immune responses in the proinflammatory milieu of celiac disease
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DOI：
10.1189/jlb.0709471
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发表时间：
2010-05-01
影响因子：
5.5
通讯作者：
Sanz, Y.
中科院分区：
文献类型：
--
作者：
De Palma, G.;Cinova, J.;Sanz, Y.
CD是一种小肠慢性炎症性疾病，存在于麸质消费后的遗传易感个体中。在这项研究中，确定了双歧杆菌（两歧双歧杆菌IATA-ES 2和长双歧杆菌ATCC 15707）和革兰氏阴性菌（脆弱拟杆菌DSM 2451、大肠杆菌CBL 2和从CD患者分离的志贺氏菌CBD 8）单独和在CD触发物（醇溶蛋白和/或IFN-γ）存在下对PBMC的表面标志物表达和细胞因子产生的影响。还在PBMC和Caco-2细胞的共培养物中评价了这些作用。革兰氏阴性菌比双歧杆菌菌株诱导更高的Th 1型促炎细胞因子（IL-12和/或IFN-γ）分泌。志贺菌CBD 8和E. coliCBL 2主要上调参与Th 1活化的HLA-DR和CD 40的表达，双歧杆菌则上调CD 83的表达。还检测到所研究的细菌、醇溶蛋白和IFN-γ之间的特异性相互作用，其有利于CD免疫特征。因此，肠道细菌可能是调节CD患者中招募到粘膜的单核细胞对麦胶蛋白和IFN-γ应答的能力的额外因素，从而影响疾病的进程。J. Leukoc. 87：765-778; 2010.
CD is a chronic inflammatory disorder of the small intestine that presents in genetically predisposed individuals following gluten consumption. In this study, the effects of Bifidobacterium (Bifidobacterium bifidum IATA-ES2 and Bifidobacterium longum ATCC15707) and Gram-negative bacteria (Bacteroides fragilis DSM2451, Escherichia coli CBL2, and Shigella CBD8 isolated from CD patients), alone and in the presence of CD triggers (gliadins and/or IFN-gamma) on surface marker expression and cytokine production by PBMCs, were determined. These effects were also evaluated in cocultures of PBMCs and Caco-2 cells. The Gram-negative bacteria induced higher secretion of Th1-type proinflammatory cytokines (IL-12 and/or IFN-gamma) than the Bifidobacterium strains. Shigella CBD8 and E. coli CBL2 up-regulated mainly HLA-DR and CD40 expression involved in Th1 activation, and Bifidobacterium strains up-regulated CD83 expression. Specific interactions among the studied bacteria, gliadins, and IFN-gamma, which favored the CD immune features, were also detected. Therefore, intestinal bacteria could be additional factors that regulate the ability of monocytes recruited to the mucosa to respond to gliadins and IFN-gamma in CD patients, influencing the course of the disease. J. Leukoc. Biol. 87: 765-778; 2010.