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Journal of Endotoxin Research
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Toll-like receptor-dependent discrimination of streptococci

Sandra Santos-Sierra

Division of Infectious Diseases, Children's Hospital, Freiburg, Germany

Douglas T. Golenbock

Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA

Philipp Henneke

Division of Infectious Diseases, Children's Hospital, Freiburg, Germany, philipp.henneke@ uniklinik-freiburg.de

Streptococcus pneumoniae and Streptococcus agalactiae cause distinct infectious diseases in small children. Similarly, these bacteria elicit very different host-cell responses in vitro. Inactivated S. agalactiae by far exceeds S. pneumoniae in the activation of inflammatory cytokines and upstream signaling intermediates such as the MAP kinase JNK. The inflammatory response to both Streptococcus spp. is mediated by MyD88, an essential adapter protein of Toll-like receptors (TLRs), although the specific TLRs that are involved have not been fully resolved. Furthermore, during logarithmic growth, S. pneumoniae releases pneumolysin that interacts with TLR4 whereas S. agalactiae releases diacylated molecules that interact with TLR2/6. Interaction of these soluble bacterial products with their cognate TLRs is critical for limiting bacterial dissemination and and systemic inflammation in mice. This might be due, in part, to TLR-mediated apoptosis induced by these factors. In conclusion related streptococcal species induce specific events in TLR-mediated signal transduction. Comparative analysis of the host-cell response to these bacteria reveals molecules such as JNK as valuable targets for adjunctive sepsis therapy.

Key Words: S. agalactiae • S. pneumoniae • innate immunity • neonates • Toll-like receptors

Journal of Endotoxin Research, Vol. 12, No. 5, 307-312 (2006)
DOI: 10.1177/09680519060120050601
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?