Abstract
Bacterial pathogens have evolved mechanisms to resist standard host defenses and to subvert normal host machinery in order to initiate disease. Invasive bacterial pathogens are now known to interact, via biochemical crosstalk, with the host, stimulating a signal transduction cascade(s) that results in host cytoskeletal rearrangements that lead to internalization of the pathogen. Until about five years ago, virtually all bacterial uptake pathways involved the exclusive requirement for host microfilaments (MFs). Since then, internalization into host cells for several bacterial genera has been reported to require microtubules (MTs) alone or together with MFs. Despite striking differences in the host cell cytoskeletal requirements for invasion, all bacterial uptake pathways have followed a common mechanistic scheme. In this general scheme, a bacterial “invasion effector ligand(s)” interacts with an eukaryotic receptor to induce a signal transduction cascade leading ultimately to the cytoskeletal rearrangements necessary for internalization. Of special interest are the receptors and intermediary host molecules which transduce the initial bacterial signal through the host cell thereby activating cytoskeletal changes and uptake of the bacterium, intracellular survival and movement of the bacterium, and sometimes exocytic release of the pathogen. In contrast to the many plasma membrane receptors with well-documented connection to cytoskeletal microfilaments, there are only a few examples of known membrane components which are connected with the microtubular cytoskeleton.KeywordsChlamydia TrachomatisNeisseria GonorrhoeaeBacterial InvasionMycobacterium BovisUptake PathwayThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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