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J Infect Dis. 2005 Feb 15;191(4):579-87. Epub 2005 Jan 14.

Host adaptation and immune modulation are mediated by homologous recombination in Helicobacter pylori.

Author information

1
Institute of Infection, Immunity, and Inflammation, and Wolfson Digestive Diseases Centre, University of Nottingham, Queen's Medical Centre, Nottingham, United Kingdom. karen.robinson@nottingham.ac.uk

Abstract

Rearrangement of genomic DNA via homologous recombination provides an alternative mechanism of gene regulation that is essential for successful colonization of the gastric mucosa by Helicobacter pylori. Inoculation of outbred mice with the H. pylori SS1 wild-type strain elicited a T helper (Th) 2 response and established a persistent infection. In contrast, inoculation with an isogenic H. pylori strain defective for homologous recombination elicited a Th1-mediated immune response and clearance of infection within 70 days. We, therefore, demonstrate that recombination is critical for mediating persistence of a microbial pathogen through the induction of ineffective immune responses.

PMID:
15655782
DOI:
10.1086/427657
[Indexed for MEDLINE]

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