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Cigarette smoke extract disturbs mitochondria-regulated airway epithelial cell responses to pneumococci

ABSTRACT: Cigarette smoke extract disturbs mitochondria-regulated airway epithelial cell responses to pneumococci

PROVIDER: PRJNA811980 | ENA |

REPOSITORIES: ENA

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Cigarette smoke extract disturbs mitochondria-regulated airway epithelial cell responses to pneumococci

Project description:Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.

2022-05-27 | GSE197751 | GEO

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

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Human primary alveolar epithelial cells (hAEC) exposed to cigarette smoke extract

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Mitochondrial mutations in cigarette smoke extract-chronically treated human oral OKF6 cells

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Temporal transcriptional response of endothelial cells to aqueous cigarette smoke extract exposure

Project description:Endothelial cells (HUVEC) were exposed to cigarette smoke extract for 3, 7, and 24 hours. Total RNA was isolated and used for hybridisation to dual channel oligonucleotide genome-wide microarrays using untreated HUVEC as a control. The objective was to find out what genes are regulated by exposure to cigarette smoke extract, and the time dependency of their regulation Keywords: time course, stress response

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Mitochondrial mutations in cigarette smoke extract-chronically treated human oral OKF6 cells

Project description:The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. The objective of this study was to analyze the mitochondrial mutations induced by chronic cigarette smoke extract treatment in human oral immortal OKF6 cells. 2 samples were included, a control passaged human oral immortal OKF6 cells and cigarette smoke extract-treated OKF6 cells. The chronic treatment for cigarette smoke extract is 7 months. Genomic DNAs were extracted from both cells and then used for Affymetix MitoChip Version 2.0 analysis.

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NHBE exposed to cigarette smoke

Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course

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Human airway epithelial responses to rhinovirus infection and cigarette smoke extract alone and in combination

Project description:This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16. The data show marked alterations in rhinovirus-induced expression profiles of a number of genes in the presence of cigarette smoke extract (CSE).

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Kentucky assay: cigarette smoke

Project description:Kentucky assay: cigarette smoke

| PRJNA626542 | ENA

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

Project description:Human alveolar epithelial cells were exposed to cigarette smoke extract (CSE) for 1, 3 and 5 weeks at 1%, 5% and 10%, and gene expression was evaluated by complete transcriptome microarrays. In this study we explored the effect of cigarette smoke on the gene expression profile. Human alveolar epithelial cells stimulated with three different concentractions of CSE (1%, 5% and 10%) and for 1, 3 and 5 weeks were used for RNA extraction and hybridization on Affymetrix microarrays.

2016-02-16 | E-GEOD-77942 | biostudies-arrayexpress

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