Dissemination mechanism of a clinical emergent bacterial pathogen

What is it about?

Serratia marcescens is an opportunistic bacterial pathogen with increasing incidence in clinical settings. Little is known about the strategies brought into play by Serratia to defeat host immune responses while propagating and disseminating its progeny. Upon invasion of non-phagocytic cells, Serratia survives and multiplies within autophagosome-like vacuoles. Serratia manipulates canonical cellular traffic pathways and the Serratia-containing vacuole (SeCV) circumvents progression into acidic, degradative compartments, avoiding elimination. In this work, we show that ShlA pore-forming toxin (PFT) expression induces a mechanism that allows Serratia to escape from the host cell.

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Photo by National Cancer Institute on Unsplash

Photo by National Cancer Institute on Unsplash

Why is it important?

Certain pathogens benefit from co-opting host intracellular compartments in the course of infection. However, after using these compartments to survive and replicate, they need to disperse progeny to prosper in a new niche. In this work, we disclose the strategy used by Serratia marcescens to command its egress from non-phagocytic cells. We show that, by the sole expression of a pore-forming toxin, intravacuolar Serratia is able to trigger a calcium signal that remodels the host cell cytoskeleton dynamics. This pathogen-promoted activity pushes the bacterial vacuolar load out of the cell in an exocytic-like process. This is the first report of a pore-forming toxin engaged in a pathogen-driven process that allows bacteria to achieve freedom without compromising host cell integrity.

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