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Infection and Immunity, December 2006, p. 6739-6749, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.00954-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Differential Role of CbpA and PspA in Modulation of In Vitro CXC Chemokine Responses of Respiratory Epithelial Cells to Infection with Streptococcus pneumoniae{triangledown}

Rikki M. A. Graham and James C. Paton*

School of Molecular and Biomedical Science, University of Adelaide, Adelaide, South Australia 5005, Australia

Received 15 June 2006/ Returned for modification 30 August 2006/ Accepted 13 September 2006

Respiratory epithelial cells play an active part in the host response to respiratory pathogens, such as Streptococcus pneumoniae, by releasing chemokines responsible for neutrophil recruitment. In order to investigate the role of specific pneumococcal virulence factors in eliciting CXC chemokine responses, type II pneumocytes (A549) and nasopharyngeal cells (Detroit-562) were infected with S. pneumoniae D39 or mutants lacking choline-binding protein A (CbpA), pneumococcal surface protein A (PspA), or specific domains thereof. In response to wild-type D39, both A549 and Detroit-562 cells showed a significant increase in CXC chemokine mRNA and interleukin-8 protein. This response was increased twofold when a cbpA deletion mutant ({Delta}CbpA) was used, suggesting that CbpA inhibits CXC chemokine induction. All three N-terminal domains of CbpA are required for this effect, as in-frame deletion of the respective region of cbpA had the same effect on the CXC chemokine response as deletion of cbpA altogether. Infection with a pspA deletion mutant ({Delta}PspA) led to a twofold decrease in the CXC chemokine response of A549 but not Detroit-562 cells, compared to infection with D39 at 2 h. Thus, PspA appears to have the ability to stimulate early CXC chemokine release from A549 cells. Deletion of the region of pspA encoding the first N-terminal {alpha}-helical domain reduced the ability of S. pneumoniae to elicit a chemokine response to the same degree as deletion of pspA altogether. Thus, the N termini of CbpA and PspA exert differential effects on CXC chemokine induction in epithelial cells infected with S. pneumoniae.

* Corresponding author. Mailing address: School of Molecular and Biomedical Science, University of Adelaide, Adelaide, SA 5005, Australia. Phone: 61-8-83035929. Fax: 61-8-83033262. E-mail: james.paton{at}adelaide.edu.au.

{triangledown} Published ahead of print on 25 September 2006.

Editor: J. N. Weiser

Infection and Immunity, December 2006, p. 6739-6749, Vol. 74, No. 12
0019-9567/06/$08.00+0     doi:10.1128/IAI.00954-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Mahdi, L. K., Ogunniyi, A. D., LeMessurier, K. S., Paton, J. C. (2008). Pneumococcal Virulence Gene Expression and Host Cytokine Profiles during Pathogenesis of Invasive Disease. Infect. Immun. 76: 646-657 [Abstract] [Full Text]  
  • Bootsma, H. J., Egmont-Petersen, M., Hermans, P. W. M. (2007). Analysis of the In Vitro Transcriptional Response of Human Pharyngeal Epithelial Cells to Adherent Streptococcus pneumoniae: Evidence for a Distinct Response to Encapsulated Strains. Infect. Immun. 75: 5489-5499 [Abstract] [Full Text]  


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