期刊
FEBS JOURNAL
卷 281, 期 19, 页码 4495-4505出版社
WILEY-BLACKWELL
DOI: 10.1111/febs.12958
关键词
Helicobacter pylori; nitroreductase; nitrosative stress; nitrosoglutathione; S-nitrosoglutathione (GSNO) reductase
资金
- Fundacao para a Ciencia e Tecnologia [PEst-OE/EQB/LA0004/2011, PTDC/BBB-BQB/0937/2012, SFRH/BD/81192/2011]
- Fundação para a Ciência e a Tecnologia [PTDC/BBB-BQB/0937/2012, SFRH/BD/81192/2011] Funding Source: FCT
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.
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