Complement C5a Induces Pro-inflammatory Microvesicle Shedding in Severely Injured Patients.
Ontology highlight
ABSTRACT: Initially underestimated as platelet dust, extracellular vesicles are continuously gaining interest in the field of inflammation. Various studies addressing inflammatory diseases have shown that microvesicles (MVs) originating from different cell types are systemic transport vehicles carrying distinct cargoes to modulate immune responses. In this study, we focused on the clinical setting of multiple trauma, which is characterized by activation and dysfunction of both, the fluid-phase and the cellular component of innate immunity. Given the sensitivity of neutrophils for the complement anaphylatoxin C5a, we hypothesized that increased C5a production induces alterations in MV shedding of neutrophils resulting in neutrophil dysfunction that fuels posttraumatic inflammation. In a mono-centered
SUBMITTER: Karasu E
PROVIDER: S-EPMC7492592 | biostudies-literature | 2020
REPOSITORIES: biostudies-literature
ACCESS DATA