Delayed cGAS-STING activation facilitates S. Typhimurium ST313 intracellular survival in iron stressed macrophages

Résumé fourni par la source

Bloodstream infections are among the leading causes of mortality from infectious diseases worldwide. In sub-Saharan Africa, multidrug-resistant Salmonella enterica serovar Typhimurium Sequence Type 313 (ST313) predominantly causes invasive non-typhoidal Salmonella infections. ST313 exhibits enhanced survival within macrophages, requiring adaptation to host iron restriction for successful dissemination. However, whether macrophage iron restriction alters ST313 iron acquisition and host cGAS-STING-mediated immune responses remains unknown. Here, we hypothesized that iron limitation in macrophages drives ST313 survival by upregulating bacterial iron acquisition genes and attenuating host cGAS-STING-mediated inflammatory signaling. This study expands our understanding of nutritional immunity by demonstrating that macrophage iron restriction modulates innate immune signaling alongside limiting bacterial access to iron. These findings provide novel mechanistic insight into the pathogenesis of invasive non-typhoidal Salmonella bloodstream infections, establishing a clear rationale for exploring iron-regulated immune pathways as host-directed therapeutic targets

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