Thromb Haemost 2005; 94(02): 266-277
DOI: 10.1160/TH05-04-0235
Theme Issue Article
Schattauer GmbH

Mechanism and consequences of invasion of endothelial cells by Staphylococcus aureus

Bhanu Sinha
1   Institute of Medical Microbiology, University Hospital of Münster, Münster
,
Mathias Herrmann
2   Institute of Medical Microbiology and Hygiene, University of Saarland, Homburg; Germany
› Author Affiliations
Further Information

Publication History

Received: 05 April 2005

Accepted after major revision: 01 July 2005

Publication Date:
05 December 2017 (online)

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Summary

It has become clear that Staphylococcus aureus is a facultative intracellular microorganism. Adherence and invasion are a prerequisite for endovascular infections caused by S. aureus, such as infective endocarditis. These phenomena may also be involved in the pathogenesis of invasive and metastatic infection upon hematogenous dissemination, such as osteomyelitis and abscess formation. The underlying molecular mechanism has been elucidated in detail, including its likely relevance in vivo. However, the mode of action of recently identified modulators of invasion, such as pls/Pls have not yet been clarified. The potential outcome for host cells and S. aureus following invasion are diverse. Surprisingly, induction of apoptosis in human endothelial cells is more complex than previously thought, since it appears to involve multiple virulence factors. In the light of increasing resistance to antimicrobial therapy, understanding the multifacetted pathogenesis of S. aureus infection in detail is needed for a better prevention and therapy.