Fig. 8: The model for the induction of proinflammatory SASP by typhoid toxin. | Nature Communications

Fig. 8: The model for the induction of proinflammatory SASP by typhoid toxin.

From: Mitochondrial injury induced by a Salmonella genotoxin triggers the proinflammatory senescence-associated secretory phenotype

Fig. 8

Typhoid toxin’s mechanism of action involves its entry into the mitochondria, where it initiates the proinflammatory SASP by directly targeting mitochondrial DNA (mtDNA) and inducing damage to this essential genetic material. This mtDNA damage triggers a cascade of events, beginning with the disruption of mtDNA integrity, which subsequently leads to mitochondrial dysfunction and a disturbance in redox homeostasis. As a consequence of these perturbations, damaged mtDNA is released into the cytosol, activating the cGAS-STING signaling pathway. This activation, in turn, instigates the expression of proinflammatory components, ultimately contributing to the development of the proinflammatory SASP (Created with BioRender.com).

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