Staphylococcus aureus and innate immunity

Abstract

Sepsis is an old and lethal disease caused by immune dysfunction in response to infection. The innate immune system is the first responder to infection and the first to dysfunction. It comprises both humoral and cellular components such as the complement, coagulation and fibrinolytic cascade systems as well as the polymorphonuclear neutrophils and monocytes. These usually recognize and respond to pathogens in an orderly fashion, leading to resolution of infection and restored homeostasis. However, in sepsis the response is first exaggerated and later reduced or even non-existent. As of today, patients suffering from sepsis only receive antibiotic and supportive treatment. The Gram-positive bacterium Staphylococcus aureus is a frequent cause of infection and sepsis. It is well known for its wide antibiotic resistance and ability to survive within humans. Several membrane-bound and secreted proteins promote staphylococcal infection by inactivating complement, surviving within phagocytes and exploiting coagulation to disseminate with the host. However, an overview of the mechanisms and virulence factors involved is currently not found. This review therefore covers documented interactions between S. aureus and the complement system, the coagulation and fibrinolytic systems as well as neutrophils and monocytes in infection and sepsis following a brief introduction to each topic. The aim is to give both the reader and the writer an overview of the current knowledge and ongoing research.