Outer inflammatory protein a (OipA) of Helicobacter pylori is regulated by host cell contact and mediates CagA translocation and interleukin-8 response only in the presence of a functional cag pathogenicity island type IV secretion system
- Resource Type
- Authors
- Danielle N, Horridge; Allison A, Begley; June, Kim; Neeraja, Aravindan; Kexin, Fan; Mark H, Forsyth
- Source
- Pathogens and disease. 75(8)
- Subject
- Antigens, Bacterial
Genomic Islands
Helicobacter pylori
Interleukin-8
bacterial infections and mycoses
Bacterial Adhesion
Helicobacter Infections
Type IV Secretion Systems
Protein Transport
Bacterial Proteins
Cell Line, Tumor
Host-Pathogen Interactions
Humans
RNA, Messenger
Amplified Fragment Length Polymorphism Analysis
Bacterial Outer Membrane Proteins
Research Article
- Language
- ISSN
- 2049-632X
OipA is a phase-variable virulence factor of Helicobacter pylori. Mutations in oipA to turn the gene phase on in a cag pathogenicity island (PAI)-negative strain of H. pylori (J68) or phase off in a cag PAI-positive strain (26695) demonstrated that phase on oipA alleles in both strains had both increased oipA mRNA and human gastric adenocarcinoma (AGS) cell adherence compared to isogenic oipA phase off mutants. An oipA phase off mutant of H. pylori 26695 demonstrated decreased IL-8 secretion by AGS cells and failure to translocate the cag PAI effector CagA. Increased attachment by OipA expressing cag PAI-negative H. pylori J68 failed to alter secreted IL-8 levels. Thus, OipA is necessary but not sufficient for the induction of IL-8; however, it is necessary for translocation of the oncoprotein CagA. Perhaps the nearly invariant phase on status of oipA alleles among cag PAI-positive H. pylori isolates relates to the role of this outer membrane protein in effective translocation of CagA. oipA mRNA comparisons between AGS cell-adherent and non-adherent H. pylori 26695 revealed significantly greater levels in the adherent cells. This may allow H. pylori to adapt to conditions of host cell contact by altering expression of this virulence factor.