Potential Compounds as Inhibitors of Staphylococcal Virulence Factors Involved in the Development of Thrombosis

TL;DR

This review explores how staphylococcal virulence factors contribute to thrombosis and identifies potential compounds that could inhibit these harmful effects.

Contribution

The paper provides a comprehensive overview of virulence factors in staphylococci and highlights potential inhibitors for thrombosis-related complications.

Findings

Staphylococcus aureus virulence factors disrupt immune responses and increase thrombosis risk.

Toxins and exoenzymes damage endothelial barriers, promoting thromboembolism.

Potential inhibitors of these virulence factors are discussed as therapeutic options.

Abstract

For many years, staphylococci have been detected mainly in infections of the skin and soft tissues, organs, bone inflammations, and generalized infections. Thromboembolic diseases have also become a serious plague of our times, which, as it turns out, are closely related to the toxic effects of staphylococci. Staphylococcus aureus, because of the presence of many different kinds of virulence factors, is capable of manipulating the host’s innate and adaptive immune responses. These include toxins and cofactors that activate host zymogens and exoenzymes, as well as superantigens, which are highly inflammatory and cause leukocyte death. Coagulases and staphylokinases can control the host’s coagulation system. Nucleases and proteases inactivate various immune defense and surveillance proteins, including complement components, peptides and antibacterial proteins, and surface receptors that are important for leukocyte chemotaxis. On the other hand, secreted toxins and exoenzymes are proteins that disrupt the endothelial and epithelial barrier as a result of cell lysis and disintegration of linking proteins, which ultimately increases the risk of thromboembolism. In this review, we discuss various virulence factors and substances that may inhibit their activity.

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