Adenosine from a biologic source regulates neutrophil extracellular traps (NETs).
作者： Kai Xu , Kimberly A. Cooney , Eric Y. Shin , Lanfang Wang , Juline N. Deppen
DOI: 10.1002/JLB.3VMA0918-374R
关键词: Agonist 、 Neutrophil extracellular traps 、 Extracellular 、 Adenosine 、 Ectonucleotidase 、 Cell biology 、 Stromal cell 、 Tissue homeostasis 、 Elastase 、 Biology
摘要: Neutrophil extracellular traps (NETs) are implicated in autoimmune, thrombotic, malignant, and inflammatory diseases; however, little is known of their endogenous regulation under basal conditions. Inflammatory effects neutrophils modulated by purines such as adenosine (ADO) that inhibitory or ATP generally up-regulates effector functions. In order to evaluate the ADO on NETs, human were isolated from peripheral venous blood healthy donors stimulated make NETs. Treatment with inhibited NET production quantified 2 methods: SYTOX green fluorescence neutrophil elastase (HNE)-DNA ELISA assay. Specific receptor agonist antagonist tested for production. The 2A (A2A R) CSG21680 NETs a similar degree ADO, whereas A2A R ZM241385 prevented ADO's NET-inhibitory effects. Additionally, CD73 membrane bound ectonucleotidase expressed mesenchymal stromal cells (MSCs) allows manipulation tissues bone marrow. MSCs formation evaluated coculture. reduced CD73-dependent manner. These results imply purine balance may locally regulate NETosis be actively maintain tissue homeostasis.
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