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Staphylococcus aureus, a prominent human pathogen, exhibits a remarkable ability to interact with host proteins involved in crucial physiological pathways, such as the complement system, coagulation cascade, and fibrinolysis cascade. This paper explores the ability of this notable bacteria to successfully manipulate and evade the host innate system, expatiating on the strategies that enhance its pathogenicity leading to implications on the healthcare system such as the propagation of diverse nosocomial infections. The investigation focuses on key S. aureus proteins, including Coagulase (Coa), von Willebrand factor-binding protein (vWbp), and Staphylokinase (SAK), which play pivotal roles in blood coagulation, fibrinolysis, and evasion of host antibacterial peptides. Notably, these proteins contribute to the formation of fibrin networks, protecting the bacterium from immune clearance and promoting lethal bloodstream infections in murine models. Additionally, the debate surrounding the role of SAK as a critical virulence factor is addressed, emphasizing its impact on biofilm formation, invasion of internal organs, and bacterial loads in sepsis studies. Furthermore, the interaction of S. aureus with matrix metalloproteinases and the secretion of superantigen-like proteins (SSL1 and SSL5) are explored as additional mechanisms employed by the bacterium to impede immune responses. In addressing emerging challenges in innate immunity, the paper discusses the escalating antibiotic resistance in S. aureus, with a specific focus on methicillin-resistant strains (MRSA) and its capacity to instigate healthcare-associated infections as an effect.
Bisola et al. (Wed,) studied this question.