Audibert C, Burucoa C, Janvier B, Fauchère J L
Laboratoire de Microbiologie A, CHU La Milétrie, 86021 Poitiers Cedex, France.
Infect Immun. 2001 Mar;69(3):1625-9. doi: 10.1128/IAI.69.3.1625-1629.2001.
Helicobacter pylori virulence is associated with the presence of the cag pathogenicity island (PAI). The cag PAI is involved in the ability to induce interleukin-8 (IL-8) secretion by human cells, which is implicated in the inflammatory response of the gastric mucosa to H. pylori infection. The aim of this study was to determine whether the genetic structure of the cag PAI is conserved and whether it is linked to IL-8 induction ability. Detection of specific markers (cagA, picB, cag13-cag14, virD4, and IS605) by PCR and dot blot hybridization and long-distance PCR determination of the presence of cagI, cagII, and the middle region of the cag PAI were performed on 153 strains isolated from adults suffering from ulcers (n = 79) or gastritis (n = 74). IL-8 induction ability was evaluated by coculture of the strains with HEp-2 cells. Eighty-three strains (54.3%) had an entire cag PAI, 12 strains (7.8%) had the cag PAI split in two, 49 strains (32%) had no cag PAI, and 9 strains exhibited other structural combinations. The presence of an entire cag PAI was statistically correlated with the presence of IS605 (P = 0.006) and the ability to induce IL-8 secretion but not with clinical presentation of the infection. The structure of the cag PAI appears to be rather conserved and is related to the proinflammatory power of a strain. The existence of strains inducing IL-8 secretion regardless of the cag PAI structure suggests that this region is not the only requirement for IL-8 secretion.
幽门螺杆菌的毒力与细胞毒素相关基因致病岛（cag PAI）的存在有关。cag PAI参与诱导人细胞分泌白细胞介素-8（IL-8）的能力，这与胃黏膜对幽门螺杆菌感染的炎症反应有关。本研究的目的是确定cag PAI的基因结构是否保守，以及它是否与IL-8诱导能力相关。通过聚合酶链反应（PCR）和斑点杂交检测特定标志物（cagA、picB、cag13 - cag14、virD4和IS605），并通过长距离PCR确定cagI、cagII以及cag PAI中间区域的存在情况，对从患有溃疡（n = 79）或胃炎（n = 74）的成人中分离出的153株菌株进行检测。通过将菌株与HEp - 2细胞共培养来评估IL-8诱导能力。83株菌株（54.3%）具有完整的cag PAI，12株菌株（7.8%）的cag PAI分裂成两部分，49株菌株（32%）没有cag PAI，9株菌株表现出其他结构组合。完整cag PAI的存在与IS605的存在（P = 0.006）以及诱导IL-8分泌的能力在统计学上相关，但与感染的临床表现无关。cag PAI的结构似乎相当保守，并且与菌株的促炎能力有关。无论cag PAI结构如何，都存在诱导IL-8分泌的菌株，这表明该区域不是IL-8分泌的唯一必要条件。
