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Review
. 2009 Mar;23(1):17-34.
doi: 10.1016/j.idc.2008.10.003.

Host defense and pathogenesis in Staphylococcus aureus infections

Frank R DeLeo  1 , Binh An Diep, Michael Otto
Affiliations
Review

Host defense and pathogenesis in Staphylococcus aureus infections

Frank R DeLeo et al. Infect Dis Clin North Am. 2009 Mar.

Abstract

Staphylococcus aureus is the most abundant cause of bacterial infections in the United States. As such, the pathogen has devised means to circumvent destruction by the innate immune system. Neutrophils are a critical component of innate immunity and the primary cellular defense against S aureus infections. This article reviews human neutrophil function in the context of S aureus virulence mechanisms and provides an overview of community-associated methicillin-resistant S aureus pathogenicity.

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Figures

Fig. 1
Fig. 1
PMN phagocytosis and microbicidal activity. Bacteria are destroyed by NADPH oxidase-derived ROS and antimicrobial proteins released from granules after phagocytosis by neutrophils. FCR, Fc receptor; CR, complement receptor; MPO, myeloperoxidase. Reproduced with permission, from M.T. Quinn, M.C.B. Ammons and F.R. DeLeo, 2006, Clinical Science, 111, 1-20 (ref. [39]). © the Biochemical Society.
Fig. 2
Fig. 2
Two possible outcomes of bacteria-neutrophil interaction. Phagocytosis of bacteria triggers production of ROS and degranulation. These processes work collectively to kill ingested bacteria, after which neutrophils undergo apoptosis and are removed by macrophages. This process promotes healthy resolution of infection (top panel). Alternatively, bacterial pathogens cause neutrophil lysis or delay apoptosis, and thereby survive and cause disease (bottom panel).Reproduced with permission, from M.T. Quinn, M.C.B. Ammons and F.R. DeLeo, 2006, Clinical Science, 111, 1-20 (ref. [39]). © the Biochemical Society.
See this image and copyright information in PMC

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