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Infection and Immunity, August 2006, p. 4841-4848, Vol. 74, No. 8
0019-9567/06/$08.00+0     doi:10.1128/IAI.00026-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Streptococcus pneumoniae Infection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2

Isabel Herrmann,¹ Markus Kellert,¹ Hauke Schmidt,² Alexander Mildner,² Uwe K. Hanisch,² Wolfgang Brück,² Marco Prinz,^2, and Roland Nau^1*,

Department of Neurology, Georg August University, D-37075 Göttingen, Germany,¹ Department of Neuropathology, Georg August University, D-37075 Göttingen, Germany²

Received 5 January 2006/ Returned for modification 9 March 2006/ Accepted 9 May 2006

The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG_35-55) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG_35-55 injection but was more severe in animals infected 7 days after the first MOG_35-55 injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

Editor: V. J. DiRita

M.P. and R.N. contributed equally to this study.

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