In this study, an in-vitro model of human airway epithelial cells (AWCs) was used to investigate the effects of exposure to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The focus of the investigation was to identify the effects of CSE on mitochondrial function. Therefore, the levels of oxidative stress as an indicator of mitochondrial stress were quantified upon CSE and Sp treatment. In addition, the expression of selected proteins was quantified and transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with the mitochondrial function.
It was observed that CSE exposure substantially altered mitochondrial function in ACEs and could decrease the physical epithelial barrier function. Moreover, CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp.
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