Post-immunisation gastritis and Helicobacter infection in the mouse: a long term study
AuthorSutton, P; Danon, SJ; Walker, M; Thompson, LJ; Wilson, J; Kosaka, T; Lee, A
PublisherBRITISH MED JOURNAL PUBL GROUP
University of Melbourne Author/sSutton, Philip
Document TypeJournal Article
CitationsSutton, P., Danon, S. J., Walker, M., Thompson, L. J., Wilson, J., Kosaka, T. & Lee, A. (2001). Post-immunisation gastritis and Helicobacter infection in the mouse: a long term study. GUT, 49 (4), pp.467-473. https://doi.org/10.1136/gut.49.4.467.
Access StatusAccess this item via the Open Access location
Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1728471
C1 - Journal Articles Refereed
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.
KeywordsImmunology not elsewhere classified; Prevention - Biologicals (e.g. Vaccines)
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