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<p>In immunocompetent hosts, <i>Salmonella enterica</i> serovar Typhimurium typically causes transient intestinal blooms with acute diarrhoea, followed by asymptomatic systemic carriage with intermittent reactivation. Inflammation elicited by bistable expression of type III secretion systems and pathogen-associated signals shapes <i>Salmonella</i> pathogenesis in both the intestine and systemic tissues. Inflammation is a two-sided coin that, over time, can either benefit or harm the host, microbiota and <i>Salmonella</i>. The host deploys the inflammasome, hypoxia and reactive oxygen and nitrogen species in both intestinal and systemic tissues, but the effectors of these responses are cell-specific and tissue-specific. <i>Salmonella</i> fine-tunes its metabolism and virulence programmes in response to chemical and physical cues derived from the microbiota and from heterogeneous host cells that vary in embryonic origin, architecture and activation states. Similar to its host, <i>Salmonella</i> undergoes coordinated virulence, metabolic, redox and energetic reprogramming with outcomes tailored to specific host cells and tissues. Paradoxically, <i>Salmonella</i> often exploits common signalling and metabolic pathways to support rapid growth in the gut lumen and in the cytosol of enterocytes while sustaining an energy-conserving and metabolic-conserving survival strategy in viscera. In this Review, I discuss current perspectives of how the dynamic interplay between microbial competition, host defences and <i>Salmonella</i> countermeasures determines the outcome of infection ranging from acute gastroenteritis to quiescent chronic infection.</p>

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Host–microbiota–pathogen interactions drive Salmonella enterica serovar Typhimurium pathogenesis

  • 期刊论文

  • 发表日期：

    2026年7月23日

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  • Andrés Vázquez-Torres

摘要

In immunocompetent hosts, Salmonella enterica serovar Typhimurium typically causes transient intestinal blooms with acute diarrhoea, followed by asymptomatic systemic carriage with intermittent reactivation. Inflammation elicited by bistable expression of type III secretion systems and pathogen-associated signals shapes Salmonella pathogenesis in both the intestine and systemic tissues. Inflammation is a two-sided coin that, over time, can either benefit or harm the host, microbiota and Salmonella. The host deploys the inflammasome, hypoxia and reactive oxygen and nitrogen species in both intestinal and systemic tissues, but the effectors of these responses are cell-specific and tissue-specific. Salmonella fine-tunes its metabolism and virulence programmes in response to chemical and physical cues derived from the microbiota and from heterogeneous host cells that vary in embryonic origin, architecture and activation states. Similar to its host, Salmonella undergoes coordinated virulence, metabolic, redox and energetic reprogramming with outcomes tailored to specific host cells and tissues. Paradoxically, Salmonella often exploits common signalling and metabolic pathways to support rapid growth in the gut lumen and in the cytosol of enterocytes while sustaining an energy-conserving and metabolic-conserving survival strategy in viscera. In this Review, I discuss current perspectives of how the dynamic interplay between microbial competition, host defences and Salmonella countermeasures determines the outcome of infection ranging from acute gastroenteritis to quiescent chronic infection.