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Infection and Immunity, November 2001, p. 6881-6886, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6881-6886.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Effect of Deficiency of Tumor Necrosis Factor Alpha or Both of Its Receptors on Streptococcus pneumoniae Central Nervous System Infection and Peritonitis

Andreas Wellmer,1 Joachim Gerber,1 Jasmin Ragheb,1 Gregor Zysk,2 Tammo Kunst,1 Alexander Smirnov,1 Wolfgang Brück,3 and Roland Nau1,*

Departments of Neurology1 and Neuropathology,3 University of Göttingen, Göttingen, and Institute of Medical Microbiology and Hygiene, University of Düsseldorf, Düsseldorf,2 Germany

Received 4 December 2000/Returned for modification 28 February 2001/Accepted 20 August 2001

Tumor necrosis factor alpha (TNF-alpha ) and TNF-beta are key mediators in bacterial inflammation. We therefore examined the role of TNF-alpha and its two receptors in murine pneumococcal central nervous system infection. TNF-alpha knockout mice and age- and sex-matched controls and TNF receptor (p55 and p75)-deficient mice and heterozygous littermates were infected intracerebrally with a Streptococcus pneumoniae type 3 strain. Mice were monitored until death or were killed 36 h after infection. Bacterial titers in blood, spleen, and brain homogenates were determined. Leukocyte infiltration and neuronal damage were assessed by histological scores. TNF-alpha -deficient mice died earlier than the controls after intracerebral infection although overall survival was similar. TNF-alpha deficiency did not inhibit leukocyte recruitment into the subarachnoid space and did not lead to an increased density of bacteria in brain homogenates. However, it caused a substantial rise of the concentration of S. pneumoniae cells in blood and spleen. Spleen bacterial titers were also increased in p55- and p75-deficient mice. TNF receptor-deficient mice showed decreased meningeal inflammation. Neuronal damage was not affected by either TNF-alpha or TNF receptor deficiency. In a murine model of pneumococcal peritonitis, 102 CFU of S. pneumoniae produced fatal peritonitis in TNF-alpha -deficient, but not wild-type, mice. Early leukocyte influx into the peritoneum was impaired in TNF-alpha -deficient mice. The lack of TNF-alpha or its receptors renders mice more susceptible to S. pneumoniae infections.

* Dept. of Neurology, University of Göttingen, Robert-Koch-Str. 40, D-37075 Göttingen, Germany. Phone: 49-551-398455. Fax: 49-551-398405. E-mail: rnau{at}gwdg.de.

Infection and Immunity, November 2001, p. 6881-6886, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6881-6886.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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