Table 1.
Major virulent mechanisms of Agr-related toxins
| 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] |
| -High concentration:Cytolytic against leuckocytes, keratinocytes, and erythrocytes | [31, 35] | |||
| 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 | [37, 38] |
| -Platelets aggregation | [39] | |||
| -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 | [41, 42] |
| -Activate TNFR1 | [43] |