Host adaptation and immune modulation are mediated by homologous recombination in Helicobacter pylori.
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.
Robinson
Karen
K
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
Loughlin
Michael F
MF
Potter
Rebecca
R
Jenks
Peter J
PJ
D000222:Adaptation, Physiological; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D049109:Cell Proliferation; D016207:Cytokines / Q000096:biosynthesis; D015964:Gene Expression Regulation, Bacterial; D016481:Helicobacter Infections / Q000276:immunology* / Q000382:microbiology*; D016480:Helicobacter pylori / Q000235:genetics* / Q000276:immunology / Q000472:pathogenicity; D008213:Lymphocyte Activation; D051379:Mice; D009154:Mutation; D011995:Recombination, Genetic
D000907:Antibodies, Bacterial; D016207:Cytokines