Summary auto-generated
This study examined how RNAIII, a regulatory RNA in Staphylococcus aureus, controls bacterial adherence to fibrinogen, fibronectin, platelets, and endothelial cells. Researchers compared a wild-type S. aureus strain (8325-4) with an RNAIII mutant (WA400) under both static and flow conditions. The RNAIII mutant showed increased adherence to fibrinogen under static conditions and enhanced ability to induce platelet aggregation, but decreased adherence to fibronectin and endothelial cells under both conditions. When endothelial cells were pre-treated with platelet-rich plasma, bacterial adherence increased substantially, especially with PMA-activated platelets. Blockade of platelet glycoprotein IIb-IIIa with tirofiban reduced adherence of both strains. The findings indicate that RNAIII down-regulates fibrinogen binding while up-regulating fibronectin and endothelial cell binding. Platelets enhance bacterial adherence to endothelial cells, but this effect is suppressed by RNAIII, likely through its regulation of fibrinogen-binding adhesins that serve as bridging molecules between bacteria, platelets, and endothelial cells.
Key findings
- RNAIII increases S. aureus adherence to fibronectin and endothelial cells while decreasing adherence to fibrinogen under static conditions
- The RNAIII mutant induces stronger platelet aggregation than the wild-type strain, correlating with increased fibrinogen binding
- Activated platelets enhance S. aureus adherence to endothelial cells, with the RNAIII mutant showing greater sensitivity to this effect
- Fibrinogen serves as a bridging molecule between bacteria, platelets, and endothelial cells in promoting adherence
- Platelet glycoprotein IIb-IIIa receptor engagement is critical for the adhesion-promoting effects of activated platelets on endothelial cells
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Abstract
In the present study, the adherence of Staphylococcus aureus (strain 8325-4) and its RNAIII mutant (WA400) to immobilised fibrinogen and fibronectin, and to human endothelial cells (EC), was studied. [3H]Thymidine-labelled bacteria in stationary phase were incubated on the test surfaces for 20 min under static or flow (200/s) conditions. The results showed: (a) increased adherence of the RNAIII mutant to fibrinogen under static conditions, and decreased adherence of the mutant to fibronectin and EC under both static and flow conditions compared with the parental strain; (b) stronger ability of the mutant compared with the parental strain to induce platelet aggregation in suspension; (c) greater adherence of the parental strain and the mutant to EC pre-treated with platelet-rich plasma compared with platelet-poor plasma, and to EC pre-treated with platelet-poor plasma compared with control; (d) increased adherence of S. aureus to EC pre-treated with PMA-activated platelets and decreased adherence to EC pre-treated with tirofiban, a platelet glycoprotein IIb-IIIa inhibitor, which paralleled with increased adherence of PMA-activated platelets and decreased adherence of glycoprotein IIb-IIIa-blocked platelets to EC in the absence of bacteria; and (e) adherence of the mutant was more sensitive to pre-treatment of EC with plasma and PMA-activated platelets. In conclusion, RNAIII down-regulates S. aureus adherence to fibrinogen under static condition and up-regulates S. aureus adherence to fibronectin and EC under both static and flow conditions. The potentiating role of activated platelets in the presence of plasma in S. aureus adherence to EC is down-regulated by RNAIII, probably due to down-regulation of adherence to fibrinogen, the important plasma protein bridging S. aureus, platelets and EC.