Quantitative Analysis of Inflammatory and Immune Responses in Dogs with Gastritis and Their Relationship toHelicobacterspp. Infection

Author:

Wiinberg Bo,Spohr Anette,Dietz Hans Henrik,Egelund Thomas,Greiter‐Wilke Andrea,McDonough Sean P.,Olsen John,Priestnall Simon,Chang Yung Fu,Simpson Kenneth W.

Abstract

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

Publisher

Wiley

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