Mas receptor activation attenuates allergic airway inflammation via inhibiting JNK/CCL2-induced macrophage recruitment

Defective absorption of acute allergic airway inflammation is involved in the initiation and development chronic asthma. After allergen exposure, there a rapid recruitment macrophages around airways, which promote inflammatory responses. The Ang-(1?7)/Mas receptor axis reportedly plays protective roles various tissue remodeling processes vivo. However, exact role Mas their underlying mechanisms during pathology remains unclear. We investigated asthma explored its vitro, aiming to find critical molecules signal pathways. expression was assessed ovalbumin (OVA)-induced asthmatic murine model. Then we estimated anti-inflammatory vivo expressions several known cytokines as well phosphorylation levels MAPK functions were studied further human bronchial epithelial cell line (16HBE). decreased inflammation. Multiplex immunofluorescence co-localized EpCAM, indicated that may function epithelium. Activating through AVE0991 significantly alleviated macrophage infiltration inflammation, accompanied with down-regulation CCL2 Further studies 16HBE showed pre-treatment inhibited LPS-induced or anisomycin-induced increase THP-1 migration via JNK Our findings suggested activation attenuated dependent recruitments pathways, receptor, phospho-JNK could be potential targets against