Particulate matter(10)-induced airway inflammation and fibrosis can be regulated by chitinase-1 suppression

BACKGROUND: Particulate matter(10) (PM(10)) can induce airway inflammation and fibrosis. Recently, chitinase-1 has been shown to play key roles in inflammation and fibrosis. We aimed to investigate the effects of chitinase-1 inhibitor in PM(10)-treated murine mice models. METHODS: In female BALB/c mice, PM(10) was intranasally administered six times over 3 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 the last week were intraperitoneally administered. Two days after the last challenges, mice were euthanized. Messenger RNA sequencing using lung homogenates was conducted to evaluate signaling pathways. RESULTS: PM(10) and/or OVA-induced airway inflammation and fibrosis murine models were established. CPX and dexamethasone ameliorated PM(10) or PM(10)/OVA-induced airway hyper-responsiveness, airway inflammation, and fibrosis. CPX and dexamethasone also reduced levels of various inflammatory markers in lung homogenates. PM(10) and OVA also induced changes in mRNA expression across an extreme range of genes. CPX and dexamethasone decreased levels of mRNA expression especially associated with inflammation and immune regulation. They also significantly regulated asthma and asthma-related pathways, including the JACK-STAT signaling pathway. CONCLUSIONS: Chitinase-1 suppression by CPX can regulate PM(10)- and OVA-induced and aggravated airway inflammation and fibrosis via an asthma-related signaling pathway. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12931-023-02392-8.