Particulate Matter10-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

Particulate matter10 (PM10) can induce airway inflammation and fibrosis. Chitinase-1 is recently known to have key roles in inflammation and fibrosis. We aimed to investigate the effects of chitinase-1 inhibitor in PM10-treated murine models. PM10 and/or OVA-induced airway inflammation and fibrosis murine models were well established. CPX and dexamethasone ameliorated PM10 or PM10/OVA-induced airway hyper-responsiveness, airway inflammation, and fibrosis. CPX and dexamethasone also reduced levels of various inflammatory markers including chitinase-1 in lung homogenates. PM10 and OVA also induced extreme changes of mRNA expression. CPX and dexamethasone decreased levels of mRNA expression especially associated with inflammation and immune regulation. They also significantly regulated asthma and asthma related pathway including JACK-STAT signaling pathway.Chitinase-1 suppression by CPX can regulate PM10-induced and aggravated airway inflammation and fibrosis via various signaling pathway. In female BALB/c mice, PM10 was intranasally administered four times over 2 weeks, and ovalbumin (OVA) was intraperitoneally injected and then intranasally administered. Chitinase-1 inhibitor (CPX) 6 times over 3 weeks or dexamethasone 3 times in last week were treated intraperitoneally. After 2 days from the last challenges, mice were sacrificed. Full RNA sequencing using lung homogenates was conducted to evaluate signaling pathway.