Characterization of virulence factors of mouse-adapted Helicobacter pyloristrain SS1 and effects on gastric hydrophobicity

Gastric infection with Helicobacter pylori results in chronic active gastri tis and in some individuals is associated with complications such as peptic ulceration and gastric cancers. A balance between bacterial factors and ho st responses may determine disease outcome. The mouse-adapted H. pylori str ain SS1 has been utilized as a model to study disease pathogenesis. Althoug h chronic gastritis is observed in this murine model of H. pylori infection , other complications of disease seen in the human host (such as peptic ulc eration) are not identified. The objectives of this study were to character ize virulence factors of the mouse-adapted H. pylori strain SS1 and determi ne host responses to infection. Vacuolating cytotoxin activity of H. pylori strain SS1 was determined after incubation of HEp-2 cells with culture sup ernatant for 24 hr. Polymerase chain reaction was performed to detect the p resence of the cagA and cagE genes. Chemokine responses from human gastric epithelial cells infected with H. pylori SS1 were assessed by measurement o f the concentration of interleukin-8 in cell-free supernatants. C57BL/6 and gld mice were infected with strain SS1 or sham-infected. Eight weeks follo wing infection, gastric tissues were obtained for histological analysis and surface hydrophobicity was measured by axisymmetric drop-shape analysis. H . pylori strain SS1 was cytotoxin negative, cagA positive, and cagE positiv e, but induced only a modest interleukin-8 response (684 +/- 140 pg/ml) fro m AGS gastric epithelial cells in comparison to a clinical isolate (4170 +/ - 410 pg/ml, P < 0.0005). Increased inflammation was observed in the stomac hs of H. pylori strain SS1-infected animals compared to uninfected controls . Gastritis was not associated with any disease complications. Despite muco sal inflammation, infected mice did not demonstrate alterations in gastric surface hydrophobicity (42.2<degrees> +/- 2.2 degrees and 41.4 degrees +/- 3.2 degrees for C57BL/6 and gld, respectively) compared to uninfected mice (43.2 degrees +/- 2.3 degrees and 39.5 degrees +/- 1.6 degrees, respectivel y). In conclusion, murine infection with H. pylori SS1, which contains puta tive bacterial virulence factors, results in gastric inflammation. However, the mucosal changes are not associated with alterations in surface hydroph obicity. Therefore, the mouse model of infection with H. pylori, strain SS1 may not serve as an entirely appropriate model to study host factors assoc iated with disease complications.