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Inhibition of ROS and upregulation of inflammatory cytokines by FoxO3a promotes survival against Salmonella typhimurium
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Inhibition of ROS and upregulation of inflammatory cytokines by FoxO3a promotes survival against Salmonella typhimurium
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Journal Article
Inhibition of ROS and upregulation of inflammatory cytokines by FoxO3a promotes survival against Salmonella typhimurium
2016
Overview
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.
FoxO3a signalling has limited influence over acute bacterial infection. Here the authors show that FoxO3a promotes survival of mice in response to chronic
Salmonella
typhimurium infection by restraining oxidative stress and ERK signalling.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ Animals
/ Forkhead Box Protein O3 - genetics
/ Forkhead Box Protein O3 - metabolism
/ Gene Expression Regulation - physiology
/ Humanities and Social Sciences
/ Mice
/ Reactive Oxygen Species - antagonists & inhibitors
/ Salmonella Infections, Animal - immunology
/ Salmonella Infections, Animal - microbiology
/ Salmonella typhimurium - pathogenicity
/ Science
