Reciprocal changes in trefoil 1 and 2 expression in stomachs of mice with gastric unit hypertrophy and inflammation

• Published in: The Journal of pathology Vol. 207; no. 1; pp. 43 - 52
• Main Authors: Franic, TV, van Driel, IR, Gleeson, PA, Giraud, AS, Judd, LM
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.09.2005
• Subjects: Animals; Autoimmune Diseases - metabolism; Cytokines - biosynthesis; Cytokines - genetics; Cytokines - physiology; Disease Models, Animal; Gastric Mucosa - metabolism; Gastric Mucosa - pathology; gastrin; Gastrins - blood; Gastritis - metabolism; Gene Expression Regulation; H(+)-K(+)-Exchanging ATPase - deficiency; H(+)-K(+)-Exchanging ATPase - genetics; hypergastrinaemia; Hyperplasia - metabolism; Hypertrophy - metabolism; IL-11; inflammation; Interleukin-11 - biosynthesis; Interleukin-11 - genetics; Interleukin-11 - physiology; metaplasia; Mice; Mice, Inbred BALB C; Mice, Mutant Strains; Mucins - genetics; Mucins - metabolism; Mucins - physiology; Muscle Proteins - genetics; Muscle Proteins - metabolism; Muscle Proteins - physiology; Peptides - genetics; Peptides - metabolism; Peptides - physiology; RNA, Messenger - genetics; Species Specificity; trefoil; Trefoil Factor-1; Trefoil Factor-2
• ISSN: 0022-3417; 1096-9896
• DOI: 10.1002/path.1811

H+/K+‐ATPase β‐subunit‐deficient mice (129/Sv background) display numerous pathologies in the stomach. Expression of the mutation in BALB/cCrSlc mice results in the development of an aberrant ‘mucus‐rich’ cell population. ‘Mucus‐rich’ cells have been described in stomachs of mice with autoimmune gastritis, a disease mediated by CD4+ T cells. Other pathological features of autoimmune gastritis are similar to those in H+/K+ β‐deficient mice and include a mononuclear cell infiltrate in the gastric mucosa, non‐functional or absent parietal cells, depletion of zymogenic cells, hypergastrinaemia, and gastric unit hypertrophy caused by immature cell hyperplasia. The present study investigates further the aberrant gastric ‘mucus‐rich’ cell lineage and analyses the mRNA expression of mucus cell products TFF1 and TFF2. ‘Mucus‐rich’ cells stained for both acidic and neutral mucins, and with a TFF2‐specific antibody. Stomachs from both models expressed decreased TFF1 mRNA and reciprocally increased TFF2 mRNA. The involvement of gastrin in regulating trefoil mRNA expression was also investigated using gastrin‐deficient mice. In contrast to previous findings, gastrin did not positively regulate TFF1 mRNA expression, but there was possible augmentation of TFF2. Additionally, a clear role for inflammation was established involving both polymorphonuclear and mononuclear cells in these models, and a link was found between mucosal hypertrophy and increased interleukin‐11 (IL‐11) expression. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.