Recent reports have highlighted the pivotal role of Ca2+ during host cell infection by bacterial pathogens. Here, we review how bacterial pore-forming toxins (PFTs) trigger global Ca2+ signals to regulate cell adhesion-, inflammatory- or death processes. We comment recent reports describing the role of bacterial effectors injected by a type III secretion system (T3SS) as well as host cell players in the formation of Ca2+ microdomains during Shigella invasion and Chlamydia extrusion of host cells. We discuss how modeling and comparison between bacterial-induced and physiological Ca2+ microdomains provides insight into the critical parameters shaping the duration of local Ca2+ responses.
Keywords: Ca(2+) modeling; Host-pathogen interactions; Membrane contact sites; Secreted toxins; Shigella.
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