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Long‐Standing Gastric Mucosal Barrier Dysfunction in Helicobacter pylori ‐Induced Gastritis in Mongolian Gerbils
Author(s) -
Sun YiQian,
Söderholm Johan D.,
Petersson Fredrik,
Borch Kurt
Publication year - 2004
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1083-4389.2004.00227.x
Subject(s) - antrum , gastritis , helicobacter pylori , barrier function , medicine , gastroenterology , helicobacter , paracellular transport , gastric mucosa , chronic gastritis , stomach , histology , intestinal permeability , ussing chamber , permeability (electromagnetism) , pathology , chemistry , biology , secretion , biochemistry , membrane , microbiology and biotechnology
Background and Aims. Helicobacter pylori infection causes chronic gastritis and leads to peptic ulcer and gastric adenocarcinoma. An impaired gastric mucosal barrier could be involved in these processes. Our aim was to investigate gastric barrier function in H. pylori ‐induced gastritis. Methods. Stripped gastric mucosal tissues of H. pylori ‐infected Mongolian gerbils (4 weeks and 70 weeks after inoculation, respectively) and controls were mounted in Ussing chambers. 51 Cr‐EDTA (paracellular probe) and horseradish peroxidase (HRP, protein antigen) were used to assess mucosal barrier function. The electrophysiological parameters of the mucosa (transepithelial potential, short circuit current, and transepithelial resistance) were monitored as measurements of barrier integrity and viability. Tissue histology was performed to assess inflammation. Results. In the antrum, both short‐term gastritis [4.68 (3.88–5.74) × 10 −6 vs. control 2.86 (2.34–3.77) × 10 −6 cm/s, p < .001] and gastritis of long‐standing [5.72 (3.88–10.94) × 10 −6 cm/s, p < .001 vs. control] showed increased permeability to 51 Cr‐EDTA. In long‐standing antral gastritis there was also an increased HRP flux [9.01 (2.98–45.02) vs. control 0.52 (0.06–1.20) pmol/h/cm 2 , p < .001]. In the corpus, permeability to 51 Cr‐EDTA was increased only in long‐standing gastritis [4.63 (3.64–7.45) × 10 −6 vs. control 2.86 (2.12–3.98) × 10 −6 cm/s, p < .01]. Gastric mucosal permeability to 51 Cr‐EDTA was correlated to histological inflammation and inflammatory activity. The levels of serum anti‐ H. pylori immunoglobulin G were positively correlated to HRP flux and 51 Cr‐EDTA permeation. Conclusions. Helicobacter pylori ‐induced gastritis in Mongolian gerbils was associated with a long‐standing gastric mucosal barrier dysfunction. The barrier defect extended from the antrum into the corpus over time. This impaired barrier function may contribute to perpetuation of chronic inflammation and may be involved in H. pylori ‐associated carcinogenesis.