Uncivil engineers: Chlamydia, Salmonella and Shigella alter cytoskeleton architecture to invade epithelial cells.
The obligate intracellular bacterial pathogen Chlamydia trachomatis is a major cause of blindness and sexually transmitted diseases. Like the enteric pathogens Salmonella and Shigella, Chlamydia injects effector proteins into epithelial cells to initiate extensive remodeling of the actin cytoskeleton at the bacterial attachment site, which culminates in the engulfment of the bacterium by plasma membrane extensions. Numerous Salmonella and Shigella effectors promote this remodeling by activating Rho GTPases and tyrosine kinase signaling cascades and by directly manipulating actin dynamics. Recent studies indicate that similar host-cell alterations occur during Chlamydia invasion, but few effectors are known. The identification of additional Chlamydia effectors and the elucidation of their modes of function are critical steps towards an understanding of how this clinically important pathogen breaches epithelial surfaces and causes infection.
Dunn
Joe Dan
JD
Department of Molecular Genetics & Microbiology & Center for Microbial Pathogenesis Duke University Medical Center, 272 Jones Building, Box 3580, Durham, NC 27710, USA.
Valdivia
Raphael H
RH
D002692:Chlamydia trachomatis / Q000472:pathogenicity*; D003599:Cytoskeleton / Q000378:metabolism*; D004705:Endocytosis; D004847:Epithelial Cells / Q000382:microbiology*; D006801:Humans; D008954:Models, Biological; D012475:Salmonella / Q000472:pathogenicity*; D012760:Shigella / Q000472:pathogenicity*; D037521:Virulence Factors / Q000378:metabolism*
D037521:Virulence Factors