Helicobacter pyloriOuter Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γSignaling
Outer membrane proteins (OMPs) can induce an immune response. Omp18 (HP1125) ofH. pyloriis a powerful antigen that can induce significant interferon-γ(IFN-γ) levels. Previous studies have suggested that IFN-γplays an important role inH. pyloriclearance. However,H. pylorihas multiple mechanisms to avoid host immune surveillance for persistent colonization. We generated anomp18mutant (H. pylori26695 andH. pyloriSS1) strain to examine whether Omp18 interacts with IFN-γand is involved inH. pyloricolonization. qRT-PCR revealed that IFN-γinduced Omp18 expression. qRT-PCR and western blot analysis revealed reduced expressions of virulence factors CagA and NapA inH. pylori26695 with IFN-γtreatment, but they were induced in the Δomp18strain. In C57BL/6 mice infected withH. pyloriSS1 and the Δomp18strain, the Δomp18strain conferred defective colonization and activated a stronger inflammatory response. Signal transducer phosphorylation and transcription 1 (STAT1) activator was downregulated by the wild-type strain but not the Δomp18strain in IFN-γ-treated macrophages. Furthermore, Δomp18strain survival rates were poor in macrophages compared to the wild-type strain. We concluded thatH. pyloriOmp18 has an important function influencing IFN-γ-mediated immune response to participate in persistent colonization.