The Effect of DPP10 in Smoking and Vaping Induced Apoptosis and Inflammation
Afonja, Abiola (2026) The Effect of DPP10 in Smoking and Vaping Induced Apoptosis and Inflammation. Doctoral thesis, Birmingham City University.
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Abiola Afonja PhD Thesis_Final Version_Final Award June 2026.pdf - Accepted Version Download (2MB) |
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 cell lines, whereas NFVE produced minimal effects. TNFα expression was increased at the transcriptional level but not consistently at the protein level. Exposure to all three extracts induced G1/S phase arrest, consistent with DNA damage–induced checkpoint activation. DPP10 knockdown produced a non-significant trend towards enhanced cytokine expression and late apoptosis, while overexpression showed a similar non-significant trend towards reduced response. Bcl-2 activation (Ser70 phosphorylation) was reduced in DPP10-silenced cells, suggesting a role in cell survival signalling.
Conclusions:
Cigarette smoke and vaping extracts promote epithelial inflammation and apoptosis through nicotine-dependent and -independent mechanisms. While DPP10 modulation produced only subtle effects, trends indicate a potential protective role in maintaining epithelial cell viability under oxidative stress by promoting Bcl-2 activation. These findings highlight DPP10 as a possible molecular modulator of airway epithelial resilience to smoke and vape exposure, warranting further mechanistic investigation.
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