Gram-positive bacteria, such as Listeria monocytogenes ( L. In part, this is achieved by the translocation of (proteinaceous) virulence factors–designated as effectors–into host cells by means of dedicated secretion systems. In turn, to optimize bacterial survival, replication and dissemination, pathogens evolved a myriad of mechanisms to counteract or deceive host immune surveillance systems and to exploit host responses. Pathogenic and symbiotic bacteria and their hosts are continuously engaged in an evolutionary arms race in which hosts have evolved multiple lines of defenses to cope with infection. In this review, we elaborate on reported methods and discuss recent advances and shortcomings in this area of tracking bacterial effector translocation.
Recently, the existing toolset has been expanded by newly developed state-of-the art methods to monitor bacterial effector translocation and dynamics. Various approaches have been developed to understand timing and order of effector translocation, quantities of translocated effectors and their subcellular localization upon translocation into host cells.
A comprehensive understanding of effector translocation in a spatio-temporal manner is of critical importance to gain insights into an effector’s mode of action. These effectors are translocated into host cells by means of dedicated secretion systems such as the type 3 secretion system (T3SS).
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IPIN Secure PIN and Password Safe 2.20.Bacteria-host interactions are characterized by the delivery of bacterial virulence factors, i.e., effectors, into host cells where they counteract host immunity and exploit host responses allowing bacterial survival and spreading.
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