Pathogenesis of Y. enterocolitica and Y. pseudotuberculosis in Human Yersiniosis
Mechanisms of action of the enteropathogenic yersiniae Ysc T3SS effectors (Yops) on host cell signaling and survival. As shown, membrane-bound Yersinia Yad and invasin proteins bind host cell β1-integrins, bringing the bacteria into close proximity to the host cell thereby facilitating insertion of the T3SS injectisome needle-like structure into the targeted host cell. Yops are then translocated across the host plasma membrane and into the cytoplasm, where they interact with the cytoskeleton and host cell signaling molecules. YopO/YpkA interacts directly with the cytoskeleton, as well as the small GTPase signaling molecules, RhoA, Rac1, and Cdc42. YopE inhibits the activities of RhoA, Rac1, and Cdc42. YopP/J promotes LPS-induced host cell apoptosis and directly induces capsase-1 cleavage. YopP/J also inhibits mitogen-activated protein kinases (MAPK) and IKK-mediated NF-κB activation, which prevents expression of proinflammatory and cell survival genes. YopM forms a complex with Rsk and Pkn in the host cell nucleus, which is believed to contribute to bacterial pathogenesis. The figure was produced using Pathway Builder 1.0, a cell signaling drawing tool provided through the Protein Lounge (http://www.ProteinLounge.com).
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