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Clinical Microbiology Reviews, July 2005, p. 521-540, Vol. 18, No. 3
0893-8512/05/$08.00+0     doi:10.1128/CMR.18.3.521-540.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Recognition of Staphylococcus aureus by the Innate Immune System

Bénédicte Fournier1* and Dana J. Philpott2

Laboratoire des Listeria,1 Groupe d'Immunité Innée et Signalisation, Institut Pasteur, Paris, France2

The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus.

* Corresponding author. Mailing address: Laboratoire des Listeria, Institut Pasteur, 25, rue du Docteur Roux, 75724 Paris Cedex 15, France. Phone: (33) 1 40 61 31 12. Fax: (33) 1 40 61 35 67. E-mail: bfournie{at}pasteur.fr.

Clinical Microbiology Reviews, July 2005, p. 521-540, Vol. 18, No. 3
0893-8512/05/$08.00+0     doi:10.1128/CMR.18.3.521-540.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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