How methicillin-resistant Staphylococcus aureus evade neutrophil killing.
OBJECTIVE
Methicillin-resistant strains of the important human pathogen Staphylococcus aureus pose a significant public health threat in the community, as they are easily transmitted, especially prone to cause invasive disease, and infect otherwise healthy individuals. The mechanistic basis for the ability of these organisms to evade the innate immune responses remains incompletely defined.


RESULTS
The success of pathogens such as S. aureus rests, in part, on their capacity to overcome neutrophil-mediated host defense to establish infection and cause human disease. S. aureus has the potential to thwart effective neutrophil chemotaxis, and phagocytosis, and succeeds in evading killing by neutrophils. Furthermore, S. aureus surviving within neutrophils promotes neutrophil cytolysis, with release of host-derived molecules that promote local inflammation. Here, we provide a brief overview of our understanding of the mechanisms by which S. aureus - including methicillin-resistant S. aureus - avoids neutrophil-mediated host defense and causes disease.


CONCLUSIONS
Understanding the molecular mechanisms by which S. aureus avoids neutrophil-mediated responses and initiates signaling cascades that culminate in neutrophil lysis will provide insights prerequisite to the development of novel targets for treating staphylococcal infections.
aInflammation Program bDepartment of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa cVeterans Administration Medical Center, Iowa City, Iowa dLaboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA.
Mallary
M
Greenlee-Wacker
Frank R
FR
DeLeo
William M
WM
Nauseef
D000818:Animals; D002633:Chemotaxis / Q000276:immunology*; D006801:Humans; D057131:Immune Evasion; D055624:Methicillin-Resistant Staphylococcus aureus / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology* / Q000473:pathology; D010587:Phagocytosis; D013203:Staphylococcal Infections / Q000276:immunology* / Q000473:pathology