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Title:
Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium | Nature Immunology
Description:
The role of type I interferon in bacterial infection is poorly understood. Sad and colleagues demonstrate that Salmonella-triggered production of type I interferon induces macrophage necroptosis, evasion of the immune response and dissemination of bacteria. Salmonella enterica serovar Typhimurium (S. Typhimurium) is a virulent pathogen that induces rapid host death. Here we observed that host survival after infection with S. Typhimurium was enhanced in the absence of type I interferon signaling, with improved survival of mice deficient in the receptor for type I interferons (Ifnar1−/− mice) that was attributed to macrophages. Although there was no impairment in cytokine expression or inflammasome activation in Ifnar1−/− macrophages, they were highly resistant to S. Typhimurium–induced cell death. Specific inhibition of the kinase RIP1 or knockdown of the gene encoding the kinase RIP3 prevented the death of wild-type macrophages, which indicated that necroptosis was a mechanism of cell death. Finally, RIP3-deficient macrophages, which cannot undergo necroptosis, had similarly less death and enhanced control of S. Typhimurium in vivo. Thus, we propose that S. Typhimurium induces the production of type I interferon, which drives necroptosis of macrophages and allows them to evade the immune response.
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description:The role of type I interferon in bacterial infection is poorly understood. Sad and colleagues demonstrate that Salmonella-triggered production of type I interferon induces macrophage necroptosis, evasion of the immune response and dissemination of bacteria. Salmonella enterica serovar Typhimurium (S. Typhimurium) is a virulent pathogen that induces rapid host death. Here we observed that host survival after infection with S. Typhimurium was enhanced in the absence of type I interferon signaling, with improved survival of mice deficient in the receptor for type I interferons (Ifnar1â/â mice) that was attributed to macrophages. Although there was no impairment in cytokine expression or inflammasome activation in Ifnar1â/â macrophages, they were highly resistant to S. Typhimuriumâinduced cell death. Specific inhibition of the kinase RIP1 or knockdown of the gene encoding the kinase RIP3 prevented the death of wild-type macrophages, which indicated that necroptosis was a mechanism of cell death. Finally, RIP3-deficient macrophages, which cannot undergo necroptosis, had similarly less death and enhanced control of S. Typhimurium in vivo. Thus, we propose that S. Typhimurium induces the production of type I interferon, which drives necroptosis of macrophages and allows them to evade the immune response.
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