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Infection and Immunity, March 2008, p. 1122-1127, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01066-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Peritoneal Challenge Modulates Expression of Pneumococcal Surface Protein C during Bacteremia in Mice{triangledown}

Lisa R. Quin,1 Quincy C. Moore III,1 Justin A. Thornton,1,{dagger} and Larry S. McDaniel1,2,3*

Departments of Microbiology,1 Surgery,2 Medicine, The University of Mississippi Medical Center, Jackson, Mississippi 392163

Received 2 August 2007/ Returned for modification 29 August 2007/ Accepted 16 December 2007

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 Streptococcus pneumoniae D39 collected from blood expressed significantly more PspC than did D39 collected from the peritoneum of intraperitoneally (i.p.)-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 i.p. with HI-D39 or PDF immediately prior to intravenous (i.v.) 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 i.p. challenge led to increased expression of 33 cytokines in serum; whereas D39 i.v. challenge 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.

* Corresponding author. Mailing address: Department of Microbiology, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216. Phone: (601) 984-6880. Fax: (601) 984-1708. E-mail: LMcDaniel{at}microbio.umsmed.edu

{triangledown} Published ahead of print on 26 December 2007.

Editor: A. Camilli

{dagger} Present address: Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38105.

Infection and Immunity, March 2008, p. 1122-1127, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01066-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Dieudonne-Vatran, A., Krentz, S., Blom, A. M., Meri, S., Henriques-Normark, B., Riesbeck, K., Albiger, B. (2009). Clinical Isolates of Streptococcus pneumoniae Bind the Complement Inhibitor C4b-Binding Protein in a PspC Allele-Dependent Fashion. J. Immunol. 182: 7865-7877 [Abstract] [Full Text]  


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