Murine splenocytes induce severe gastritis and delayed-type hypersensitivity and suppress bacterial colonization in Helicobacter pylori-infected SCIDmice

The goal of this study was to evaluate the role of host immunity in gastrit is and epithelial damage due to Helicobacter pylori, Splenocytes from H, py lori-infected and uninfected C57BL/6 mice were adoptively transferred to H, pylori-infected and uninfected severe combined immunodeficient (SCID) mice . Transfer was verified by dow cytometry, and all mice were evaluated for t he presence of delayed-type hypersensitivity (DTH) by footpad inoculation w ith sterile H, pylori sonicate and for humoral immunity by enzyme-linked im munosorbent assay. The severity of gastritis and gastric epithelial damage was quantified histologically, epithelial proliferation was determined by p roliferating cell nuclear antigen staining, and colonization was quantified by culture, C57BL/6 mice, but not nonrecipient SCID mice, developed modera te gastritis in response to H, pylori, In contrast, recipient SCID mice dev eloped severe gastritis involving 50 to 100% of the gastric mucosa and stro ng DTH responses not present in C57BL/6 mice, DTH, but not serum anti-H. py lori immunoglobulin G, correlated with adoptive transfer, gastritis, and ba cterial clearance. Severe gastritis, but not bacterial colonization, was as sociated with epithelial metaplasia, erosions, and an elevated labeling ind ex, This study demonstrates that (i) adaptive immunity is essential for dev elopment of gastritis due to H, pylori in mice, (ii) T-cell-enriched lympho cytes in SCID mice induce DTH and gastritis, which is more severe than dono r gastritis, and (iii) the host inflammatory response, not direct bacterial contact, causes epithelial damage. The greater severity of gastritis in re cipient SCID mice than in donor C57BL/6 mice suggests that gastritis is due to specific T-cell subsets and/or the absence of regulatory cell subsets i n the transferred splenocytes.