Cortistatin protects against inflammatory airway diseases through curbing CCL2 and antagonizing NF-κB signaling pathway.

Asthma is a chronic inflammatory disease affecting millions of people around the world, yet much remains unknown about its underlying mechanisms. Cortistatin (CST) is a neuropeptide which is reported to be a potential endogenous anti-inflammatory factor in several conditions. To testify the potential involvement of CST in airway inflammatory reaction, an ovalbumin (OVA)-induced mice model was established in wild-type (WT) as well as CST-knockout (Cort^-/-) mice. Thereafter, lung tissue or cell samples were gathered in each group, and histological analysis as well as cell counting assay indicated that Cort^-/- mice exhibited exaggeration of asthma compared with WT control group. Moreover, mRNA sequencing assay revealed that CCL2 was a potential target of CST in asthma, and administration of CCL2 inhibitor alleviated airway inflammation of asthma in Cort^-/- mice. Moreover, NF-κB signaling pathway might be closely associated with the protective function of CST in asthma, as enhanced activation of NF-κB signaling pathway was observed in OVA-induced asthma model of Cort^-/- mice, and SN50, an inhibitor of NF-κB signaling pathway, antagonized asthma development in Cort^-/- mice. In summary, CST might represent as a promising target for the treatment of asthma through interacting with CCL2 and NF-κB signaling pathway.

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