Implication of the Structure of theHelicobacter pylori cagPathogenicity Island in Induction of Interleukin-8 Secretion

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Abstract
Helicobacter pylorivirulence is associated with the presence of thecagpathogenicity island (PAI). ThecagPAI 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 toH. pyloriinfection. The aim of this study was to determine whether the genetic structure of thecagPAI 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 thecagPAI 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 entirecagPAI, 12 strains (7.8%) had thecagPAI split in two, 49 strains (32%) had nocagPAI, and 9 strains exhibited other structural combinations. The presence of an entirecagPAI 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 thecagPAI 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 thecagPAI structure suggests that this region is not the only requirement for IL-8 secretion.