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Infection and Immunity, February 2000, p. 492-501, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Host Cellular Immune Response to Pneumococcal Lung Infection in Mice

Aras Kadioglu,1 Neill A. Gingles,1 Kate Grattan,1 Alison Kerr,2 Tim J. Mitchell,2 and Peter W. Andrew1,*

Department of Microbiology & Immunology, University of Leicester, Leicester,1 and Division of Infection & Immunity, University of Glasgow, Glasgow,2 United Kingdom

Received 17 June 1999/Returned for modification 9 September 1999/Accepted 5 November 1999

Although there is substantial evidence that pneumolysin is an important virulence factor in pneumococcal pneumonia, relatively little is known about how it influences cellular infiltration into the lungs. We investigated how the inability of mutant pneumococci to produce pneumolysin altered the pattern of inflammation and cellular infiltration into the lungs. The effect on bacterial growth in the lungs also was assessed. There were three phases of growth of wild-type bacteria in the lungs: a decline followed by a rapid increase and then stasis or decline. The absence of pneumolysin was associated with a more rapid early decline and then a much slower increase in numbers. The pattern of inflammatory-cell accumulation also had distinct stages, and the timing of these stages was influenced by the presence of pneumolysin. Neutrophils began to accumulate about 12 to 16 h after infection with wild-type pneumococci. This accumulation occurred after the early decline in pneumococcal numbers but coincided with the period of rapid growth. Following infection with pneumococci unable to make pneumolysin, neutrophil influx was slower and less intense. Coincident with the third stage of pneumococcal growth was an accumulation of T and B lymphocytes at the sites of inflammation, but the accumulation was not associated with an increase in the total number of lymphocytes in the lungs. Lymphocyte accumulation in the absence of pneumolysin occurred but was delayed.

* Corresponding author. Mailing address: Department of Microbiology & Immunology, Medical Sciences Building, University Rd., Leicester LE1 9HN, United Kingdom. Phone: (116) 2523018. Fax: (116) 2525030. E-mail: pwa{at}le.ac.uk.

Infection and Immunity, February 2000, p. 492-501, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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