Quantitative analysis of inflammatory and immune responses in dogs with gastritis and their relationship to Helicobacter spp. infection.

The present study sought to quantitatively examine mucosal inflammatory and immune responses in dogs with gastritis and the relationship of these responses to infection with Helicobacter. Gastric biopsies from 30 dogs were evaluated for B- and T-lymphocytes, neutrophils, cosinophils, macrophages, and mast cells. Mucosal atrophy, fibrosis, cellularity, and severity of gastritis were graded qualitatively. Messenger-RNA (mRNA) for actin, interleukin-1beta (IL-1beta), IL-4. IL-8, and IL-10, transforming growth factor beta (TGF-beta). and interferon gamma (IFN-gamma) was quantified by polymerase chain reaction (PCR). The presence of Helicobacter spp. was determined by urease activity, histology, PCR, and enzyme-linked immumosorbent assay. mRNA for IL-1beta, IL-8 IL-10. TGF-beta, and IFN-gamma was detected in most dogs. IL-4 mRNA was detected in only 1 dog. Correlations were observed for IL- 1beta versus IL-8 and IL-10; IL-8 versus IL-10, IFN-gamma, and TGF-beta, and IL-10 versus IFN-gamma. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-beta and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). Gastritis was categorized as lyrnphoplasmacytic in all dogs, and its histologic severity correlated with atrophy, infiltration with lymphocytes and inacrophages, and expression of IL-10 and IFN-gamma. Of the dogs examined, 76.7% were infected with Helicobacter spp. Infection was associated with increased expression of TGF-beta and fibrosis. Circulating anti -Helicobacter immunoglobulin G titers were higher in uninfected than infected dogs. We Conclude that lymphoplasruacytic gastritis in dogs is characterized by concurrent activation of proinflaminatory and inurnunomodUlatory cytokines, with increased mRNA expression related to mucosal pathology. No significant associations between Helicobacter infection and proinflaminatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.