Neutrophil-Derived Microvesicles Enhance Pulmonary Vascular Inflammation via a Toll-like Receptor 4 Signaling-Dependent Mechanism.

We have demonstrated that NMVs produced within LPS-stimulated blood are potent mediators of lung microvascular endothelial cells via monocyte-derived TNFα signaling. NMV-induced monocyte activation involves TLR4 signaling and is protease sensitive, suggesting that MVs serve as vehicles of damage-associated molecular pattern (DAMP) activity, mediated by surface proteins. Together these findings support a major role for NMVs as novel long-range mediators for systemic propagation of inflammation, contributing to the pathogenesis of sepsis-induced indirect acute lung injury. (1) Tsiridou et al. European Respiratory Journal. 2020;56:4468.