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Infect. Immun. doi:10.1128/IAI.01579-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

THE INFLUENCE OF NEUTROPENIA ON THE COURSE OF SEROTYPE 8 PNEUMOCOCCAL PNEUMONIA IN MICE

Division of Infectious Diseases, Montefiore Medical Center and Albert Einstein College of Medicine, Bronx, New York; Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York; Department of Pathology, Albert Einstein College of Medicine and Jacobi Medical Center, Bronx, New York; Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee

^* To whom correspondence should be addressed. Email: Pirofski{at}aecom.yu.edu.

	Abstract

Polymorphoneutrophils (PMNs) are important effector cells in host defense against pneumonia. However, PMNs can also induce inflammation and tissue damage. To investigate the contribution of PMNs to host defense against pneumococcal pneumonia, we determined the effect of the PMN depleting rat MAb RB6-8C5 on the survival and the inflammatory and cellular response in the lungs to a lethal intranasal infection with serotype 8 pneumococcus in Balb/c mice. Control mice received rat IgG (rIgG). Strikingly, the survival of RB6-treated mice was significantly prolonged compared to rIgG-treated mice. Although the number of lung CFUs was statistically similar in both groups 4, 24 and 32 hrs after infection, rIgG-treated mice developed higher levels of bacteremia and histopathological examination of the lungs of infected mice revealed marked differences between RB6- and rIgG-treated mice. RB6-treated mice had focal, perivascular lesions without accompanying parenchymal inflammation and rIgG-treated mice had diffuse, interstitial parenchymal inflammation. Lung homogenates from the rIgG-treated mice had more leukocytes and significantly more total and apoptotic PMNs as determined by FACS analysis with Annexin V and TUNEL staining of lung tissue samples. Studies with a pneumolysin deficient mutant of the serotype 8 strain we used also demonstrated prolonged survival of RB6- compared to rIgG-treated mice. Taken together, our findings suggest that PMNs enhance the likelihood of early death and alter the pathological response to pneumococcal lung infection in Balb/c mice with serotype 8 pneumonia without significantly affecting bacterial clearance or the cytokine response.

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