Table 1 Major virulent mechanisms of Agr-related toxins
From: The role of Staphylococcus aureus quorum sensing in cutaneous and systemic infections
Toxin (gene) | Contribution of Agr expression on genes | Molecular character | Major virulent mechanism | References |
|---|---|---|---|---|
PSMα (PSMα) | Activation (AgrA enhances PSMα promoter) | Amyloid protofilaments assembled by stacking of amphipathic helices | -Low concentration: stimulate leukocytes FPR2, leading to inflammatory response | [34] |
| Â | -High concentration:Cytolytic against leuckocytes, keratinocytes, and erythrocytes | |||
PSMβ (PSMβ) | Activation (AgrA enhances PSMβ promoter) | Unknown |  | |
δ-toxin (hld) | Activation (hld encoded in RNAIII) | Mast cell degranulation | [36] | |
α-toxin (hla) | Activation (RNAIII initiate hla translation) | Pore-forming | -Pore forming cytotoxicity via ADAM10 binding in epithelial, endothelial, and immune cells | |
| Â | Â | -Platelets aggregation | [39] | |
| Â | Â | -Inflammasome response in macrophages | [40] | |
protein A (spa) | Downregulation (RNAIII inhibit spa mRNA, RNAIII-spa mRNA degraded by RNAse III) | Five homologous Ig-binding domains | -Resist opsonization by Fc binding | |
-Activate TNFR1 | [43] |