FrxA is an S-nitrosoglutathione reductase enzyme that contributes to Helicobacter pylori pathogenicity

Marta C. Justino, Margarida R. Parente, Ivo G. Boneca, Lígia M. Saraiva

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Helicobacter pylori is a pathogen that infects the gastric mucosa of a large percentage of the human population worldwide, and predisposes to peptic ulceration and gastric cancer. Persistent colonization of humans by H. pylori triggers an inflammatory response that leads to the production of reactive nitrogen species. However, the mechanisms of H. pylori defence against nitrosative stress remain largely unknown. In this study, we show that the NADH-flavin oxidoreductase FrxA of H. pylori, besides metabolizing nitrofurans and metronidazole, has S-nitrosoglutathione reductase activity. In agreement with this, inactivation of the FrxA-encoding gene resulted in a strain that was more sensitive to S-nitrosoglutathione. FrxA was also shown to contribute to the proliferation of H. pylori in macrophages, which are key phagocytic cells of the mammalian innate immune system. Moreover, FrxA was shown to support the virulence of the pathogen upon mouse infection. Altogether, we provide evidence for a new function of FrxA that contributes to the successful chronic colonization ability that characterizes H. pylori.

Original languageEnglish
Pages (from-to)4495-4505
Number of pages11
JournalFebs Journal
Volume281
Issue number19
DOIs
Publication statusPublished - 1 Oct 2014

Keywords

  • Helicobacter pylori
  • Nitroreductase
  • Nitrosative stress
  • Nitrosoglutathione
  • S-nitrosoglutathione (GSNO) reductase

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