Yamaoka Y, Kodama T, Kita M, Imanishi J, Kashima K, Graham D Y
Department of Medicine, Veterans Affairs Medical Centre and Baylor College of Medicine, Houston, Texas, USA.
Gut. 1999 Dec;45(6):804-11. doi: 10.1136/gut.45.6.804.
It is not known whether cagA+ Helicobacter pylori in duodenal ulcer (DU) have enhanced virulence compared with non-DU cagA+ H pylori.
To investigate the relation between presentation, H pylori density, interleukin 1beta (IL-1beta) and IL-8 production, and cagA status.
Fifty DU and 50 gastritis patients with cagA+ H pylori and 11 with cagA- infections were studied. Bacterial density and cytokine production were assessed using the same biopsies. Cytokine production was also measured from supernatants of medium following coculture of H pylori with MKN-45 cells.
There was no relation between H pylori density and cagA status. There was a dose dependent relation between mucosal cytokine levels and density of cagA+ H pylori. H pylori density increased to a threshold, followed by a rapid increase in cytokines and then a plateau. IL-1beta and IL-8 levels in the antrum were greater in DU than in gastritis; in the corpus the cytokine level/H pylori differed irrespective of similar H pylori densities. However, cytokine production was similar in vitro, independent of presentation or biopsy site, suggesting that host factors are critical determinants of the inflammatory response. Mucosal IL-8 and IL-1beta levels were low with cagA- and cagA+, cagE- H pylori infections.
The increase in antral IL-1beta and IL-8 production and inflammation in DU is related to increased numbers of bacteria and not to an increase in cytokine production per cagA+ isolate. There was no evidence of enhanced virulence of H pylori from DU compared with cagA+ non-DU H pylori.
十二指肠溃疡(DU)患者体内的细胞毒素相关基因A(cagA)阳性幽门螺杆菌与非DU的cagA阳性幽门螺杆菌相比,其毒力是否增强尚不清楚。
研究临床表现、幽门螺杆菌密度、白细胞介素1β(IL-1β)和IL-8产生与cagA状态之间的关系。
对50例cagA阳性幽门螺杆菌感染的DU患者、50例cagA阳性幽门螺杆菌感染的胃炎患者以及11例cagA阴性幽门螺杆菌感染患者进行了研究。使用相同的活检组织评估细菌密度和细胞因子产生情况。幽门螺杆菌与MKN-45细胞共培养后的培养基上清液也用于测量细胞因子产生情况。
幽门螺杆菌密度与cagA状态之间无关联。黏膜细胞因子水平与cagA阳性幽门螺杆菌密度之间存在剂量依赖关系。幽门螺杆菌密度增加到一个阈值后,细胞因子迅速增加,随后达到平台期。DU患者胃窦部的IL-1β和IL-8水平高于胃炎患者;在胃体部,无论幽门螺杆菌密度相似与否,细胞因子水平/幽门螺杆菌情况均有所不同。然而,体外细胞因子产生情况相似,与临床表现或活检部位无关,这表明宿主因素是炎症反应的关键决定因素。cagA阴性和cagA阳性、cagE阴性幽门螺杆菌感染时,黏膜IL-8和IL-1β水平较低。
DU患者胃窦部IL-1β和IL-8产生及炎症增加与细菌数量增加有关,而非与每个cagA阳性菌株的细胞因子产生增加有关。没有证据表明与cagA阳性非DU幽门螺杆菌相比,DU幽门螺杆菌的毒力增强。