The Effect of DPP10 in Smoking and Vaping Induced Apoptosis and Inflammation
Abstract
Background: Cigarette smoke and electronic cigarette (vape) aerosols both induce oxidative stress and inflammation in airway epithelial cells, contributing to the development of chronic respiratory diseases. Dipeptidyl peptidase-like protein 10 (DPP10), a member of the dipeptidyl peptidase family, has been linked to asthma susceptibility and airway epithelial remodelling, yet its role in epithelial responses to smoke or vape exposure remains poorly understood. This study aimed to investigate the role of DPP10 in modulating inflammation and apoptosis in human airway epithelial cells exposed to cigarette smoke extract (CSE), nicotine-free vape extract (NFVE), and nicotine-containing vape extract (VE). Methods: Human alveolar (A549) and bronchial (Beas-2B) epithelial cells were treated with CSE, NFVE, or VE standardized for nicotine concentration. Cell viability was assessed using XTT assays to determine sub-toxic concentrations for subsequent experiments. Cytokine production (IL6, IL8, TNFα) was quantified by ELISA and gene expression by qPCR. DPP10 expression was modulated using siRNA knockdown and plasmid overexpression. Cell cycle distribution was analyzed by flow cytometry, and apoptosis was assessed through Annexin V/PI staining and Bcl-2 activation assays. Results: CSE exerted the greatest cytotoxicity, followed by VE and NFVE, with Beas-2B cells showing higher sensitivity than A549. CSE and VE significantly upregulated IL6 and IL8 gene and protein expression in both…
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Evidence Hub reads this as a thesis, done in cell cultures (in vitro), not in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health.
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