Innate immunity as a key element in host defense against methicillin resistant Staphylococcus aureus

Abstract

Methicillin resistant Staphylococcus aureus (MRSA) is a frequent reason for healthcare visits. Both pathogen and host differences likely are factors in determining the frequency of recurrent MRSA infections in otherwise normal hosts. Among such host factors are altered innate immune responses in skin and soft tissues. This review examines four selected processes of the innate immune system by which the host may prevent MRSA skin or soft tissue infections. The first involves cationic antimicrobial peptides (CAMPs) found in skin, skin organs, and leukocytes. The second requires chemotactic molecules secreted by monocytes and their derivatives. The third is CRP, a primitive opsonin and activator of complement. And the fourth includes neutrophil defenses. These last include the traditional phagocytic bacterial killing by intact neutrophils. This is an intracellular killing accomplished by reactive oxygen species (ROS), CAMPs, and microbicidal enzymes. A second recently described neutrophil defense results in extracellular killing using neutrophil extracellular traps (NETs), NETs are produced as neutrophils lyse by a process known as NETosis. The balance between these and similar innate immune responses and bacterial virulence factors likely determines whether MRSA colonization/exposure results in infection of skin or soft tissue.