Cellular mechanisms of bacterial internalization counteracted by Yersinia.

Upon host-cell contact, human pathogenic Yersinia species inject Yop virulence effectors into the host through a Type III secretion-and-translocation system. These virulence effectors cause a block in phagocytosis (YopE, YopT, YpkA, and YopH) and suppression of inflammatory mediators (YopJ). The Yops that block phagocytosis either interfere with the host cell actin regulation of Rho GTPases (YopE, YopT, and YpkA) or specifically and rapidly inactivate host proteins involved in signaling from the receptor to actin (YopH). The block in uptake has been shown to be activated following binding to Fc, Complement, and beta1-integrin receptors in virtually any kind of host cell. Thus, the use of Yersinia as a model system to study Yersinia-host cell interactions provides a good tool to explore signaling pathways involved in phagocytosis.