Inhibition of ROS and upregulation of inflammatory cytokines by FoxO3a promotes survival against Salmonella typhimurium
Julie Joseph,
Emmanuelle S. Ametepe,
Naveen Haribabu,
Gerard Agbayani,
Lakshmi Krishnan,
Alexandre Blais and
Subash Sad ()
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Julie Joseph: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Emmanuelle S. Ametepe: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Naveen Haribabu: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Gerard Agbayani: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Lakshmi Krishnan: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Alexandre Blais: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Subash Sad: Faculty of Medicine, Microbiology, and Immunology, University of Ottawa
Nature Communications, 2016, vol. 7, issue 1, 1-14
Abstract:
Abstract Virulent intracellular pathogens, such as the Salmonella species, engage numerous virulence factors to subvert host defence mechanisms to induce a chronic infection that leads to typhoid or exacerbation of other chronic inflammatory conditions. Here we show the role of the forkhead transcription factor FoxO3a during infection of mice with Salmonella typhimurium (ST). Although FoxO3a signalling does not affect the development of CD8+ T cell responses to ST, FoxO3a has an important protective role, particularly during the chronic stage of infection, by limiting the persistence of oxidative stress. Furthermore, FoxO3a signalling regulates ERK signalling in macrophages, which results in the maintenance of a proinflammatory state. FoxO3a signalling does not affect cell proliferation or cell death. Thus, these results reveal mechanisms by which FoxO3a promotes host survival during infection with chronic, virulent intracellular bacteria.
Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12748
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DOI: 10.1038/ncomms12748
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