Helicobacter pylori outer membrane vesicles modulate proliferation and interleukin-8 production by gastric epithelial cells
Helicobacter pylori outer membrane vesicles modulate proliferation and interleukin-8 production by gastric epithelial cells
复制标题
DOI：
10.1128/iai.71.10.5670-5675.2003
复制
发表时间：
2003-10-01
影响因子：
3.1
通讯作者：
Keenan, JI
中科院分区：
文献类型：
--
作者：
Ismail, S;Hampton, MB;Keenan, JI
幽门螺杆菌感染常与胃炎有关，可发展为溃疡或恶性肿瘤。临床结果的多样性部分归因于幽门螺杆菌的毒力因子和粘附素的表达。然而，幽门螺旋杆菌不一定要附着在上皮上才会引起胃炎。我们假设外膜囊泡（OMV），不断从幽门螺杆菌表面脱落，作为宿主细胞反应的独立激活剂发挥作用。在本研究中，我们发现来自cag PAI（+）产毒株和cag PAI（-）非产毒株的低剂量OMV可促进AGS胃上皮细胞的增殖。在较高剂量下，我们检测到生长停滞，毒性增加，白细胞介素-8 （IL-8）产生。检测到的唯一菌株差异是产毒株产生空泡，而cag PAI（-）非产毒株的OMV产生更高水平的IL-8。总之，我们认为组成性脱落的OMV在促进幽门螺杆菌感染相关的低级别胃炎中起作用。
Helicobacter pylori infection, which is always associated with gastritis, can progress to ulceration or malignancy. The diversity in clinical outcomes is partly attributed to the expression of virulence factors and adhesins by H. pylori. However, H. pylori may not have to adhere to the epithelium to cause gastritis. We hypothesize that outer membrane vesicles (OMV), which are constantly shed from the surface of H. pylori, play a role as independent activators of host cell responses. In this study, we found that low doses of OMV from cag PAI(+) toxigenic and cag PAI(-) nontoxigenic strains increased proliferation of AGS gastric epithelial cells. At higher doses, we detected growth arrest, increased toxicity, and interleukin-8 (IL-8) production. The only strain differences detected were vacuolation with the toxigenic strain and higher levels of IL-8 production with OMV from the cag PAI(-) nontoxigenic strain. In summary, we suggest that constitutively shed OMV play a role in promoting the low-grade gastritis associated with H. pylori infection.