Abstract
Sepsis is a devastating disease process characterized by a systemic inflammatory response in the host, evoked by a known or suspected pathogen. Staphylococcus aureus has emerged as a leading etiologic agent of sepsis, owing to its propensity to cause deep-seated tissue infection and bacteremia [1]. S. aureus harbors an arsenal of virulence factors to facilitate tissue adhesion, immune evasion, and host cell injury. In the bloodstream, these factors cause inflammation, impair immune cell function, alter coagulation, and compromise vascular integrity. This review will discuss key secreted and surface-anchored proteins required for S. aureus infection in the hostile host environment of the bloodstream, emphasizing mechanistic insights on virulence factor function that illustrate the complex nature of the host–pathogen interaction. While we currently lack a clear understanding of the temporal and spatial integration of these virulence factors in the bloodstream, it is apparent that S. aureus triggers pathophysiologic disturbances that are further amplified by the host inflammatory response, culminating in the severe clinical manifestations of sepsis and septic shock.
Highlights
The clinical manifestations of sepsis span a continuum of severity, in the most extreme form termed ‘‘septic shock,’’ in which vascular insults and systemic inflammation lead to compromised cardiac function and blood pressure, culminating in impaired oxygen delivery to the tissues and organ failure
Genetic regulatory control that leads to increased production of PantonValentine Leukocidin (PVL), phenol soluble modulins (PSMs), and a-toxin in highly virulent methicillin-resistant S. aureus (MRSA) strains has been described as a molecular mechanism that underlies increased disease severity observed upon infection with these isolates [13,14,15]
Two of the best-studied of these proteins are CHemotaxis Inhibitory Protein of Staphylococci (CHIPS) and Staphylococcal Complement INhibitor (SCIN)
Summary
The clinical manifestations of sepsis span a continuum of severity, in the most extreme form termed ‘‘septic shock,’’ in which vascular insults and systemic inflammation lead to compromised cardiac function and blood pressure, culminating in impaired oxygen delivery to the tissues and organ failure. In the bloodstream, circulating immune cells and the vascular endothelium are primary targets of staphylococcal virulence factors. Among the longest studied of these toxins are the staphylococcal superantigens that potently stimulate non-specific T-cell proliferation and activation and potentiate the host inflammatory response associated with sepsis [9].
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