Markers of anti-oxidant response in tobacco smoke exposed subjects: A data-mining review

Comandini, Alessia; Marzano, Valeria; Curradi, Giacomo; Federici, Giorgio; Urbani, Andrea; Saltini, Cesare

doi:10.1016/j.pupt.2010.05.006

Cited by 22 publications

(16 citation statements)

References 52 publications

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“…It is worth noting that our study differs from many published studies in which macrophages were isolated from lungs of patients who smoked [33], [40], [41]. In many of these studies, macrophages were profiled so that the clues to the pathogenesis of COPD could be identified.…”

Section: Discussionmentioning

confidence: 90%

Inflammatory Transcriptome Profiling of Human Monocytes Exposed Acutely to Cigarette Smoke

et al. 2012

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BackgroundCigarette smoking is responsible for 5 million deaths worldwide each year, and is a major risk factor for cardiovascular and lung diseases. Cigarette smoke contains a complex mixture of over 4000 chemicals containing 1015 free radicals. Studies show smoke is perceived by cells as an inflammatory and xenobiotic stimulus, which activates an immune response. The specific cellular mechanisms driving cigarette smoke-induced inflammation and disease are not fully understood, although the innate immune system is involved in the pathology of smoking related diseases.Methodology/Principle findingsTo address the impact of smoke as an inflammagen on the innate immune system, THP-1 cells and Human PBMCs were stimulated with 3 and 10% (v/v) cigarette smoke extract (CSE) for 8 and 24 hours. Total RNA was extracted and the transcriptome analysed using Illumina BeadChip arrays. In THP-1 cells, 10% CSE resulted in 80 genes being upregulated and 37 downregulated by ≥1.5 fold after 8 hours. In PBMCs stimulated with 10% CSE for 8 hours, 199 genes were upregulated and 206 genes downregulated by ≥1.5 fold. After 24 hours, the number of genes activated and repressed by ≥1.5 fold had risen to 311 and 306 respectively. The major pathways that were altered are associated with cell survival, such as inducible antioxidants, protein chaperone and folding proteins, and the ubiquitin/proteosome pathway.ConclusionsOur results suggest that cigarette smoke causes inflammation and has detrimental effects on the metabolism and function of innate immune cells. In addition, THP-1 cells provide a genetically stable alternative to primary cells for the study of the effects of cigarette smoke on human monocytes.

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Section: Discussionmentioning

confidence: 90%

Inflammatory Transcriptome Profiling of Human Monocytes Exposed Acutely to Cigarette Smoke

et al. 2012

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“…Because NRF2 activation is a wellestablished cellular response to environmental stressors, it has been considered as biomarker of exposure to xenobiotics. In lung, a data mining of several transcription studies followed by Ingenuity pathway analysis reported that the NRF2 signature is upregulated in healthy smokers, therefore suggesting that NRF2-regulated antioxidant genes play a central role in protection against toxic effects of tobacco smoke (Comandini et al, 2010). Similarly, the levels of NQO1, an enzyme regulated by NRF2, were 15-fold higher in liver tissue obtained from acetaminophenoverdosed patients (Aleksunes et al, 2006).…”

Section: Biomarkers As Nuclear Factor (Erythroidderived 2)-like 2mentioning

confidence: 99%

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

et al. 2018

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“…Significant normalized enrichment scores were observed after 2-h postexposure and were then sustained until 48 h with the highest score observed at 4-h postexposure time. Many of the biological functions known to be directly affected upon CS exposure, both in vivo and in vitro (7,17,37,72), were identified based on the leading edge genes To confirm the differential expression of a subset of mRNAs observed in the microarray analysis, RT-qPCR on the same RNA samples were performed. RT-qPCRs were conducted using the High-Capacity cDNA Reverse Transcription Kit and TaqMan Assay-on-Demand kits from Applied Biosystems (Darmstadt, Germany).…”

Section: Smoking Cessationmentioning

confidence: 99%

Human bronchial epithelial cells exposed in vitro to cigarette smoke at the air-liquid interface resemble bronchial epithelium from human smokers

Mathis

Poussin

Weisensee

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

137

117

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Organotypic culture of human primary bronchial epithelial cells is a useful in vitro system to study normal biological processes and lung disease mechanisms, to develop new therapies, and to assess the biological perturbations induced by environmental pollutants. Herein, we investigate whether the perturbations induced by cigarette smoke (CS) and observed in the epithelium of smokers' airways are reproducible in this in vitro system (AIR-100 tissue), which has been shown to recapitulate most of the characteristics of the human bronchial epithelium. Human AIR-100 tissues were exposed to mainstream CS for 7, 14, 21, or 28 min at the air-liquid interface, and we investigated various biological endpoints [e.g., gene expression and microRNA profiles, matrix metalloproteinase 1 (MMP-1) release] at multiple postexposure time points (0.5, 2, 4, 24, 48 h). By performing a Gene Set Enrichment Analysis, we observed a significant enrichment of human smokers' bronchial epithelium gene signatures derived from different public transcriptomics datasets in CS-exposed AIR-100 tissue. Comparison of in vitro microRNA profiles with microRNA data from healthy smokers highlighted various highly translatable microRNAs associated with inflammation or with cell cycle processes that are known to be perturbed by CS in lung tissue. We also found a dose-dependent increase of MMP-1 release by AIR-100 tissue 48 h after CS exposure in agreement with the known effect of CS on this collagenase expression in smokers' tissues. In conclusion, a similar biological perturbation than the one observed in vivo in smokers' airway epithelium could be induced after a single CS exposure of a human organotypic bronchial epithelium-like tissue culture.

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Markers of anti-oxidant response in tobacco smoke exposed subjects: A data-mining review

Cited by 22 publications

References 52 publications

Inflammatory Transcriptome Profiling of Human Monocytes Exposed Acutely to Cigarette Smoke

Inflammatory Transcriptome Profiling of Human Monocytes Exposed Acutely to Cigarette Smoke

Transcription Factor NRF2 as a Therapeutic Target for Chronic Diseases: A Systems Medicine Approach

Human bronchial epithelial cells exposed in vitro to cigarette smoke at the air-liquid interface resemble bronchial epithelium from human smokers

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