Helicobacter pyloriOuter Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γSignaling

Abstract

Outer membrane proteins (OMPs) can induce an immune response. Omp18 (HP1125) of H. pylori is a powerful antigen that can induce significant interferon-γ (IFN-γ) levels. Previous studies have suggested that IFN-γ plays an important role in H. pylori clearance. However, H. pylori has multiple mechanisms to avoid host immune surveillance for persistent colonization. We generated an omp18 mutant (H. pylori 26695 and H. pylori SS1) strain to examine whether Omp18 interacts with IFN-γ and is involved in H. pylori colonization. qRT-PCR revealed that IFN-γ induced Omp18 expression. qRT-PCR and western blot analysis revealed reduced expressions of virulence factors CagA and NapA in H. pylori 26695 with IFN-γ treatment, but they were induced in the Δomp18 strain. In C57BL/6 mice infected with H. pylori SS1 and the Δomp18 strain, the Δomp18 strain 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 Δomp18 strain in IFN-γ-treated macrophages. Furthermore, Δomp18 strain survival rates were poor in macrophages compared to the wild-type strain. We concluded that H. pylori Omp18 has an important function influencing IFN-γ-mediated immune response to participate in persistent colonization.

Comment on “Helicobacter pyloriOuter Membrane Protein 18 (Hp1125) Is Involved in Persistent Colonization by Evading Interferon-γSignaling”

“…However, we know that, in chronic process of colonization adopted by H. pylori , the connection of a unique factor to the drive of the final pattern of this phenomenon could be too speculative. Despite the interesting report of Shan et al [ 1 ], we may hypothesize more factors involved in H. pylori colonization. Surprisingly, H. pylori colonization is not comparable with that of other pathogens [ 5 ].…”

“…We read with interest the paper by Shan et al [ 1 ] in a recent issue. It is an interesting paper concluding that Helicobacter pylori ( H. pylori ) omp18 is indirectly affecting long term bacterial colonization by successfully influencing IFN- γ -mediated immune response.…”

“…To our knowledge, the host immune response to the infection is ineffective; accordingly, the bacterium persists and remains for decades. In brief, Shan et al [ 1 ] reported the oipA as a critical factor affecting bacterial colonization. However, we know that, in chronic process of colonization adopted by H. pylori , the connection of a unique factor to the drive of the final pattern of this phenomenon could be too speculative.…”

Risk factors for recurrence of Helicobacter pylori infection after successful eradication in Chinese children: A prospective, nested case‐control study

“…31,34 IFN-γ protects patients from H pylori infection and helps host remove H pylori. 35,36 37 Furthermore, this increases the body's susceptibility to H pylori infection. 40 The IFNGR1-56TT…”

In vitro and in vivo effects of suloctidil on growth and biofilm formation of the opportunistic fungus Candida albicans

“…The vaginal tissue was sliced into 5-μm thick sections for hematoxylin and eosin staining (HE) and examined by light microscopy. Inflammatory cell infiltrates (Polymorphonuclear leukocytes and mononuclear cells) in the antrum and body were graded as described: 0, none; 1, some infiltrates; 2, mild infiltrates (few aggregates in submucosa and mucosa); 3, moderate infiltrates (several aggregates in submucosa and mucosa); 4, marked infiltrates (many large aggregates in submucosa and mucosa); 5, nearly the entire mucosa contained a dense infiltrate; and 6, the entire mucosa contained a dense infiltrate [ 23 ].…”