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Infection and Immunity, April 2003, p. 1813-1819, Vol. 71, No. 4
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.4.1813-1819.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Pneumococcal Behavior and Host Responses during Bronchopneumonia Are Affected Differently by the Cytolytic and Complement-Activating Activities of Pneumolysin
Rania Jounblat,1 Aras Kadioglu,1* Tim J. Mitchell,2 and Peter W. Andrew1
Department of Microbiology and Immunology, University of Leicester, Leicester, LE1 9HN,1
Division of Infection and Immunity, University of Glasgow, Glasgow, G12 8QQ, United Kingdom2
Received 23 September 2002/
Returned for modification 22 November 2002/
Accepted 4 December 2002
Pneumolysin, a multifunctional toxin produced by all clinical isolates of Streptococcus pneumoniae, is strongly implicated in the pathogenesis of pneumococcal bronchopneumonia and septicemia. Using isogenic mutant strains, we examined the effect of deletion of the cytotoxic activity or complement-activating activity of pneumolysin on bacterial growth in lungs and blood, histological changes in infected lung tissue, and the pattern of inflammatory cell recruitment. Both of the activities of pneumolysin contributed to the pathology in the lungs, as well as the timing of the onset of bacteremia. Histological changes in the lungs were delayed after infection with either mutant compared to the changes seen after infection with the wild-type pneumococcus. The complement-activating activity of pneumolysin affected the accumulation of T cells, whereas the toxin's cytolytic activity influenced neutrophil recruitment into lung tissue.
* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Leicester, P.O. Box 138, University Rd., Leicester, LE1 9HN, United Kingdom. Phone: 44 116 2523018. Fax: 44 116 2525030. E-mail: ak13{at}le.ac.uk.
Editor: J. T. Barbieri
Infection and Immunity, April 2003, p. 1813-1819, Vol. 71, No. 4
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.4.1813-1819.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
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Copyright © 2003 by the American Society for Microbiology. All rights reserved.