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Infection and Immunity, September 2001, p. 5294-5304, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5294-5304.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Pulmonary and Systemic Host Response to Streptococcus pneumoniae and Klebsiella pneumoniae Bacteremia in Normal and Immunosuppressed Mice

Erjian Wang, Nathalie Ouellet, Marie Simard, Isabelle Fillion, Yves Bergeron, Denis Beauchamp, and Michel G. Bergeron*

Centre de Recherche en Infectiologie, Université Laval, Québec, Québec, Canada

Received 3 May 2001/Returned for modification 5 June 2001/Accepted 18 June 2001

Mortality related to bacteremic pneumonia remains high, and the role of sepsis in inflammation, pulmonary injury, and death remains unclear, mostly in leukopenic states. In the present study, the microbiology, histopathology, and host response to Streptococcus pneumoniae and Klebsiella pneumoniae infection were determined in an experimental model of bacteremia in immunocompetent and leukopenic mice. Leukocyte depletion by cyclophosphamide did not impair the early clearance of pneumococci from blood but facilitated growth in lungs. By contrast, klebsiellae rapidly grew in blood of leukopenic mice. These observations suggest that tissue-based phagocytes and circulating leukocytes, respectively, play prominent roles in S. pneumoniae and K. pneumoniae eradication. The kinetics of leukocyte recruitment in lungs during S. pneumoniae bacteremia suggested early strong inflammation in immunocompetent mice that is associated with tumor necrosis factor alpha release and histological disorders, including cell debris and surfactant in alveolar spaces. Leukocyte depletion further stimulated pulmonary capillary leakage both in S. pneumoniae and K. pneumoniae bacteremia, which seemed attributable to bacterial virulence factors. Nitric oxide production did not differ significantly among groups. Leukopenia and low platelet counts characterized the late stage of bacteremia for both strains, but only K. pneumoniae altered renal function. Understanding the pathogenesis of bacteremia will help establish beneficial therapies for both sepsis and pneumonia.

* Corresponding author. Mailing address: Centre de Recherche en Infectiologie, Centre Hospitalier de l'Université Laval, 2705 Boul. Laurier, Sainte-Foy, Québec, Canada G1V 4G2. Phone: (418) 654-2705. Fax: (418) 654-2715. E-mail: Michel.G.Bergeron{at}crchul.ulaval.ca.

Infection and Immunity, September 2001, p. 5294-5304, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5294-5304.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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