Gut 2001;49:467-473 ( October )

Article

Post-immunisation gastritis and Helicobacter infection in the mouse: a long term study P Sutton^a, S J Danon^a, M Walker^b, L J Thompson^a, J Wilson^a, T Kosaka^a, A Lee^a

^a School of Microbiology and Immunology, University of New South Wales, Sydney, NSW 2052, Australia, ^b Department of Histopathology, Imperial College School of Medicine at St Mary's, Norfolk Place, London W2 1PG, UK

Correspondence to: P Sutton, CSL Ltd, Parkville, VIC 3052 Australia. Phil_Sutton{at}csl.com.au

Accepted for publication 12 February 2001

BACKGROUND AND AIMSHelicobacter 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.
RESULTSProphylactic 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.
CONCLUSIONThe 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.


Keywords: Helicobacter; immunisation; post-immunisation gastritis

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© 2001 by Gut
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