期刊
INTERNATIONAL JOURNAL OF MEDICAL MICROBIOLOGY
卷 303, 期 8, 页码 548-552出版社
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.ijmm.2013.07.008
关键词
cagPAI pathogenicity island; I kappa Bs; Inflammation; RelA phosphorylation
资金
- German Research Foundation [SFB854 TP4, GRK1167]
Colonization of the gastric epithelium by Helicobacterpylori induces the transcription factor nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-kappa B) and the innate immune response. Virulent strains of H. pylori carry a cog pathogenicity island (cagPAI), which encodes a type IV secretion system (T4SS). Recent publications have shown controversial data regarding the role of the T4SS and the effector protein cytotoxin associated gene A (CagA), which becomes translocated by the T4SS into the eukaryotic epithelial cell, in H. pylori-induced NF-kappa B activation. Thus, this study analyses by using three different H. pylori strains (P1, B128 and G27) whether CagA is required to initiate activation of different molecules of inhibitors of kappa B (I kappa B) and the NF-kappa B transcription factor RelA. We provide experimental evidence that H. pylori induces phosphorylation of NF-KB inhibitors I kappa Bot, I kappa Bp and I kappa Bs, and degradation of IKBcz. Further, H. pylori stimulates phosphorylation of RelA at amino acids S536, S468 and S276, promotes DNA binding of RelA, and interleukin 8 (IL-8) gene expression in a T4SS-, but CagA-independent manner at early time points. (C) 2013 Elsevier GmbH. All rights reserved.
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