Peer-reviewed veterinary case report
Inflammation and immune response in dogs with gastritis
By Wiinberg, Bo et al.·Published in Journal of veterinary internal medicine·2005·Royal Veterinary and Agricultural University·View original on PubMed →
PetCaseFinder translated the abstract of this peer-reviewed paper into plain English so pet owners can read it. We do not publish original research — every detail traces back to the citation above. How we work →
Original publication title: Quantitative analysis of inflammatory and immune responses in dogs with gastritis and their relationship to Helicobacter spp. infection.
- Species:
- dog
Plain-English summary
A group of 30 dogs with gastritis (inflammation of the stomach lining) was studied to understand how their immune responses related to infection with Helicobacter bacteria. Most of the dogs showed signs of inflammation, and about 77% were found to be infected with Helicobacter. The study found that the severity of gastritis was linked to certain immune markers, but there wasn't a clear connection between the infection and the level of inflammation. Treatment options for gastritis often include dietary changes and medications to reduce stomach acid, which can help improve symptoms and manage inflammation.
People also search for: dog gastritis symptoms · Helicobacter infection in dogs · dog stomach inflammation treatment
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 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-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 immunosorbent 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-y. Mucosal pathology was related to cytokine mRNA expression (neutrophils to IL-8 and IFN-gamma, macrophages and lymphocytes to IFN-gamma, and fibrosis to IL-1beta). 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-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 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.
Find similar cases for your pet
PetCaseFinder finds other peer-reviewed reports of pets with the same symptoms, plus a plain-English summary of what was tried across them.
Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/15715041/