Effects of BabA expression during H. pylori infection of Mongolian gerbils

• Objective: Helicobacter pylori outer membrane proteins, such as the BabA adhesin are associated with severe pathological outcome.  However, the in vivo role of the BabA adhesin during long-term infection is not clear.  Design and Setting: Mongolian gerbils were inoculated with the H. pylori TN2GF4 and were necropsied at 1, 3, 6, and 18 months.  Main outcome measures: Bacterial clones recovered from the infected gerbils were evaluated by immunoblot for BabA expression, radioimmunoassay for Leb-binding, and bacterial binding to gastric tissue.  H1 antigen expression and the increase in sialylation levels were monitored by immunohistochemistry.  Results: BabA expression increased, then progressively decreased, and was completely absent by 6 months post-infection.  Loss of BabA expression was caused by nucleotide changes/deletions within the babA gene that resulted in a truncated BabA.  Infection with a BabA-expressing H. pylori caused severe mucosal injury, whereas infection with a BabA non-expressing strain caused only mild inflammation.  In response to the infection, changes in the epithelial glycosylation pattern were observed, similar to responses observed in humans and monkeys.  Conclusion: Down-regulation of BabA is probably a result of adaptation to the host response during long-term H. pylori infection.  BabA expression is most likely not essential for colonisation, but for the obtained gerbil host response, which confirms the role of BabA adhesin as a virulence factor and its impact in the induction of a severe inflammatory response.  The changes in glycosylation of gastric mucosa demonstrate the relevance of the Mongolian gerbil as a model for H. pylori infection and host responses.

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