Open AccessQuantitative Analysis of Inflammatory and Immune Responses in Dogs with Gastritis and Their Relationship to Helicobacter spp. Infection
Author(s) -
Wiinberg Bo,
Spohr Anette,
Dietz Hans Henrik,
Egelund Thomas,
GreiterWilke Andrea,
McDonough Sean P.,
Olsen John,
Priestnall Simon,
Chang Yung Fu,
Simpson Kenneth W.
Publication year - 2005
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.2005.tb02651.x
Subject(s) - medicine , gastritis , helicobacter pylori , immunology , immune system , proinflammatory cytokine , helicobacter , interleukin , fibrosis , cytokine , pathology , inflammation
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, 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 of Helicobacter spp. 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 with Helicobacter spp. Infection was associated with increased expression of TGF‐β and fibrosis. Circulating anti‐ Helicobacter immunoglobulin 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 between Helicobacter infection and proinflammatory cytokine expression, severity of gastritis, or differences in the pathogenicity of different Helicobacter spp. were found.