Infect. Immun. doi:10.1128/IAI.01066-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Peritoneal Challenge Modulates Expression of Pneumococcal Surface Protein C (PspC) during Bacteremia in Mice
Lisa R. Quin,
Quincy C. Moore III,
Justin A. Thornton,
and
Larry S. McDaniel*
Departments of Microbiology Surgery, and Medicine, The University of Mississippi Medical Center, Jackson, MS 39216
* To whom correspondence should be addressed. Email:
LMcDaniel{at}microbio.umsmed.edu.
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Abstract |
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Differential expression of pneumococcal virulence proteins has been demonstrated. We previously demonstrated challenge route-dependent differences in pneumococcal surface protein C (PspC) expression during bacteremia. In this study, we investigated differences in PspC expression during the transition of pneumococci from the peritoneum to the blood. Time-course analysis of PspC expression using flow cytometry demonstrated that S. pneumoniae D39 collected from blood expressed significantly more PspC than D39 collected from the peritoneum of intraperitoneal (IP)-infected mice. Various challenge models were then used to determine whether host responses originating from the peritoneum can influence PspC expressed by pneumococci in the blood. Using heat-inactivated D39 (HI-D39) and sterile peritoneal dialysis fluid (PDF), we investigated whether stimulation of peritoneal responses can influence PspC expression. Injection of mice IP with HI-D39 or PDF immediately prior to intravenous (IV) infection with D39 caused a significant increase in PspC expressed by D39 in the blood. Finally, we used cytokine array analysis to investigate specific inflammatory mediators that may result in differential PspC expression. Of the 96 inflammatory cytokines assayed, D39 IP led to increased expression of 33 cytokines in serum; whereas, D39 IV led to increased expression of 15 and decreased expression of 11 cytokines relative to serum of the uninfected control. These results indicate that PspC is differentially regulated during growth in vivo, and that the level of expression varies depending on the host environment.