Post-immunisation gastritis and Helicobacterinfection in the mouse: a long term study. Issue 4 (1st October 2001)

• Record Type: Journal Article
• Authors: Sutton, P; Danon, S J; Walker, M; Thompson, L J; Wilson, J; Kosaka, T; Lee, A
• Is Part Of: Gut. Volume 49:Issue 4(2001)
• Page Start: 467
• Page End: 473
• Publication Date: 2001-10-01
• Subjects: Helicobacter -- immunisation -- post-immunisation gastritis; Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.49.4.467
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : BACKGROUND AND AIMS: Helicobacter pylori is a major cause of peptic ulcers and gastric cancer. Vaccine development is progressing but there is concern that immunisation may exacerbate Helicobacter induced gastritis: prophylactic immunisation followed by challenge with H felis or H pylori can induce a more severe gastritis in mice than seen with infection alone. The aim of this study was to investigate the relationship between immunity to Helicobacter infection and post-immunisation gastritis. METHODS: (1) C57BL/6 mice were prophylactically immunised before challenge with either H felis or H pylori. Histopathology and colonisation were assessed one month post-challenge. (2) C57BL/6 mice were prophylactically immunised against H felis infection and gastritis assessed up to 18 months post-challenge. RESULTS: Prophylactic immunisation induced a reduction in bacterial colonisation following H felis challenge which was associated with increased severity of active gastritis with neutrophil infiltration and atrophy. However, immunised mice challenged with H pylori SS1 had little evidence of pathology. Long term follow up showed that post-immunisation gastritis was evident at three months. However, from six months onwards, although immunised/challenged mice still developed gastritis, there was no significant difference between inflammation in these mice and infected controls. Post-immunisation gastritis was not associated with the serum antibody response. Immunisation prevented the formation of secondary lymphoid aggregates in the gastric tissue. CONCLUSION: The H felis mouse model of post-immunisation gastritis is the most extreme example of this type of pathology. We have shown in this model that post-immunisation gastritis is a transient event which does not produce long term exacerbation of pathology.