FSTL1 aggravates cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy

Abstract Background Cigarette smoke (CS) is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD). Follistatin-like protein 1 (FSTL1), critical during embryogenesis particularly in respiratory lung development, novel mediator related to inflammation and tissue remodeling. We tried investigate the role of FSTL1 CS-induced autophagy dysregulation, airway Methods Serum specimens were obtained from COPD patients controls. Adult female wild-type (WT) mice, ± mice flox/+ exposed room air or chronic CS. Additionally, 3-methyladenine (3-MA), an inhibitor autophagy, was applied CS-exposed WT mice. The tissues serum murine models tested autophagy-associated expression by ELISA, western blotting immunohistochemical. Autophagosome observed using electron microscope technology. LTB4, IL-8 TNF-? bronchoalveolar lavage fluid examined ELISA. Airway remodeling function also assessed. Results Both biomarkers increased Autophagy activation upregulated accompanied inflammation. showed lower level compared with control can resist inflammatory response, impaired function. 3-MA pretreatment have similar manifestation Conclusions promotes modulating therefore targeting may shed light on treating cigarette smoke-induced COPD.