Figure 5
Figure 5. Scheme of the suggested mechanism of MPO-mediated PMN recruitment. Electrostatic repulsion between the negatively charged glycocalyx of PMN and the vessel wall prevents the interactions of PMN with the endothelium. Given the difference in height, the glycocalyx (∼ 500 nm) shields selectins (∼ 40 nm), which communicate the definite contact of PMN to the vessel wall (for instance, binding of constitutively expressed P-selectin glycoprotein ligand-1 [PSGL-1] on the PMN membrane with P-selectins on the endothelial surface). Thus binding of MPO to glycosaminoglycans reduces the negative surface charge and allows for electrostatic attraction of PMN to the endothelium, which then mediates receptor-ligand interactions, resulting in PMN tethering and rolling, adhesion, and diapedesis.

Scheme of the suggested mechanism of MPO-mediated PMN recruitment. Electrostatic repulsion between the negatively charged glycocalyx of PMN and the vessel wall prevents the interactions of PMN with the endothelium. Given the difference in height, the glycocalyx (∼ 500 nm) shields selectins (∼ 40 nm), which communicate the definite contact of PMN to the vessel wall (for instance, binding of constitutively expressed P-selectin glycoprotein ligand-1 [PSGL-1] on the PMN membrane with P-selectins on the endothelial surface). Thus binding of MPO to glycosaminoglycans reduces the negative surface charge and allows for electrostatic attraction of PMN to the endothelium, which then mediates receptor-ligand interactions, resulting in PMN tethering and rolling, adhesion, and diapedesis.

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