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Infect. Immun. doi:10.1128/IAI.00687-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Dynamics of N. gonorrhoeae Attachment: Microcolony Development, Cortical Plaque Formation and Cytoprotection

Department of Molecular Microbiology and Immunology, Microscopy Core Facility, and Department of Pathology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd, Portland, OR, 97239

^* To whom correspondence should be addressed. Email: somaggie{at}email.arizona.edu.

	Abstract

Neisseria gonorrhoeae is the bacterium that causes gonorrhea, a major sexually transmitted disease and a significant co-factor for HIV transmission. The retactile N. gonorrhoeae Type IV pilus (Tfp) mediates twitching motility and attachment. Using live-cell microscopy, we reveal for the first time the dynamics of twitching motility by N. gonorrhoeae on its natural environment, human epithelial cells. Bacteria aggregate into microcolonies on the cell surface and induce a massive remodeling of the microvillus architecture. Surprisingly, microcolonies are motile, and they fuse to form progressively larger structures that undergo rapid reorganization, suggesting that bacteria communicate with each other during infection. As reported, actin plaques form beneath microcolonies. Here, we show that cortical plaques co-migrate with motile microcolonies. These activities are dependent on pilT, the Tfp retraction locus. Cultures infected with a pilT mutant have significantly higher numbers of apoptotic cells, compared to cultures infected with the wt strain. Inducing pilT expression with IPTG partially rescues cells from infection-induced apoptosis, demonstrating that Tfp retraction is intrinsically cytoprotective for the host. Tfp-mediated attachment is therefore a continuum of microcolony motility and force stimulation of host cell signaling leading to a cytoprotective effect.

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