Bronchiolar epithelial catalase is diminished in smokers with mild COPD

Abstract

This study aimed to investigate bronchiolar catalase expression and its relationship with smoking and/or chronic obstructive pulmonary disease (COPD) in humans and to determine the dynamic change of bronchiolar catalase expression in response to cigarette smoke in mice.Lung tissue was obtained from 36 subjects undergoing surgery for peripheral tumours, consisting of lifelong nonsmokers and smokers with or without COPD. Male C57BL/6 mice were subjected to cigarette smoke exposure for up to 3 months followed by a 28-day cessation period. We quantified bronchiolar catalase mRNA using laser capture microdissection and quantitative reverse transcription-polymerase chain reaction. C22 club cells (Clara cells) in culture were exposed to cigarette smoke extract and monitored for viability when catalase expression was decreased by siRNA.Catalase was decreased at mRNA and protein levels in bronchiolar epithelium in smokers with COPD. In mice, bronchiolar catalase is temporarily upregulated at 1 day after cigarette smoke exposure but is downregulated by repeated cigarette smoke exposure, and is not restored long after withdrawal once emphysema is developed. Decreasing catalase expression in C22 cells resulted in greater cigarette smoke extract-induced cell death.Bronchiolar catalase reduction is associated with COPD. Regulation of catalase depends on the duration of cigarette smoke exposure, and plays a critical role for protection against cigarette smoke-induced cell damage. @ERSpublications Regulation of bronchiolar catalase in COPD depends on the duration of cigarette smoke exposure

Evaluation of salivary catalase, vitamin C, and alpha‐amylase in smokers and non‐smokers: a retrospective cohort study

“…Catalase activity decreased in the saliva of smokers compared to non‐smokers, but the difference was not statistically significant. This finding is consistent with studies by Tonguc et al , Betsuyaku et al and Arja et al , who found that catalase activity decreased significantly in the saliva of smokers compared to non‐smokers.…”

Nicotine alters mucin rheological properties

“…Like many pulmonary disorders, particularly in COPD, cigarette smoking has been shown to induce mucin hypersecretion; however, whether it directly affects mucin rheological property remains elusive. Although cigarette smoke extract has been commonly utilized in respiratory disease related studies (4,22), the complexity of its composition (more than 4,500 molecules) prevents us from identifying a clear mechanism (47). Nicotine, on other hand, is a common major addictive compound in cigarette smoke that has well-established cellular and molecular mechanisms relating to pulmonary mucus hypersecretion disorder (31).…”

Improved outcomes in ex-smokers with COPD: a UK primary care observational cohort study

“…Smoking is a major cause of chronic obstructive pulmonary disease (COPD), although individuals show differing susceptibility to smoking-related airflow limitation [1, 2] because of interacting environmental and host factors [3–5]. Smoking accelerates decline in forced expiratory volume in 1 s (FEV 1 ) in susceptible subjects [2], though physiologically defined COPD can develop in subjects with normal rates of decline who start adult life with low FEV 1 [6].…”