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Superoxide dismutase from Helicobacter pylori suppresses the production of pro‐inflammatory cytokines during in vivo infection
Author(s) -
Stent Andrew,
Every Alison L.,
Chionh Yok T.,
Ng Garrett Z.,
Sutton Philip
Publication year - 2018
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/hel.12459
Subject(s) - superoxide dismutase , helicobacter pylori , immune system , gastritis , in vivo , immunology , cytokine , inflammation , monoclonal antibody , biology , antibody , oxidative stress , microbiology and biotechnology , biochemistry , genetics
Background Helicobacter pylori has undergone considerable adaptation to allow chronic persistence within the gastric environment. While H. pylori ‐associated diseases are driven by an excessive inflammation, severe gastritis is detrimental to colonization by this pathogen. Hence, H. pylori has developed strategies to minimize the severity of gastritis it triggers in its host. Superoxide dismutase ( SOD ) is well known for its role in protecting against oxidative attack; less recognized is its ability to inhibit immunity, shown for SOD from mammalian sources and those of some bacterial species. This study examined whether H. pylori SOD (Hp SOD ) has the ability to inhibit the host immune response to these bacteria. Materials and Methods The ability of recombinant Hp SOD to modify the response to LPS was measured using mouse macrophages. A monoclonal antibody against Hp SOD was generated and injected into H. pylori ‐infected mice. Results Addition of Hp SOD to cultures of mouse macrophages significantly inhibited the pro‐inflammatory cytokine response to LPS stimulation. A monoclonal antibody was generated that was specific for SOD from H. pylori . When injected into mice infected with H. pylori for 3 months, this antibody was readily detected in both sera and gastric tissues 5 days later. While treatment with anti‐Hp SOD had no effect on H. pylori colonization at this time point, it significantly increased the levels of a range of pro‐inflammatory cytokines in the gastric tissues. This did not occur with antibodies against other antioxidant enzymes. Conclusions SOD from H. pylori can inhibit the production of pro‐inflammatory cytokine during in vivo infection.