Evaluation of mouse laryngeal inflammation upon low and high dose cigarette smoke exposures via NanoString analysis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE208079 | GEO | 2022/07/13
REPOSITORIES: GEO
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Project description:Expression data from rats exposed to cigarette smoke (CS) at three concentrations (sham, 300 µgTPM/l and 600 µgTPM/l) for 13 weeks (5d/week; 2hrs/day) after three different recovery times (2hrs, 6hrs and 20hrs after last treatment); lung tissue Keywords: recovery time course and dose dependency Male Sprague-Dawley rats were nose-only-exposed for 13 weeks in total, 5d/week, 2h/day to following concentrations of mainstream cigarette smoke from the standard reference cigarette 2R4F: sham, 300 µgTPM (Total particulate matter)/l or 600 µgTPM/l.
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Project description:Cigarette smoke (CS) is an aerosol containing more than 6,000 chemicals and one of the risk factor in the development of chronic inflammatory lung disease. To evaluate biological effect of CS on human respiratory tract, organotypic bronchial epithelial cultures can be used to replicate in vivo tissue conditions. The MucilAir organotypic bronchial epithelial cultures were exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product (NTV), which we recently developed, using a Vitrocell exposure system. This system consists of three steps: the generation of CS, dilution, and exposure to an air-liquid interface cultured cells in a specially designed module. This exposure scenario mimics CS exposure in the human airway (i.e. direct aerosol exposure to the apical surface of air-liquid interface-cultured cells), We found a dose-dependent increase in the number of differentially expressed genes following 3R4F cigarette smoke exposure, compared with expression in air-exposed controls. In contrast, no changes were detected following exposure to NTV vapor.
2018-02-09 | E-MTAB-6471 | biostudies-arrayexpress
Project description:Gene expression profiling in animal models exposed to cigarette mainstream smoke (CS) shapes up as a promising tool for investigating the molecular mechanisms involved in the onset and development of CS-related disease and may aid in the identification of disease candidate genes. Here we report on differential gene expression in lungs of rats exposed for 2, 7, and 13 weeks to 300 and 600 µg total particulate matter (TPM)/l CS with sacrifice 2, 6, or 20 h after the last exposure. The results showed a distinct, mostly transient, expression pattern of differentially expressed genes encoding antioxidant and xenobiotic-metabolizing enzymes, which confirmed and extended in qualitative and quantitative terms the findings of a former study, where rats were exposed to CS either acutely (once) or short-term (3 weeks). With increasing length of exposure, there was a distinct, mostly sustained, expression of genes implicated in innate and adaptive immune responses, clearly pointing to an emerging inflammatory response. Notably, this inflammatory response included the expression of lung disease-related genes not yet linked to CS exposure, such as osteopontin, arginase 1, and chitinase, as well as genes encoding proteolytic enzymes. Finally, our experiments also revealed a CS exposure-dependent shift in the cyclical expression of genes involved in controlling the circadian rhythm. Altogether, these results provide further insight into the molecular mechanisms of CS-dependent disease onset and development and thus may also be useful for defining CS-specific molecular biomarkers of disease. Keywords: gene expression profiling, cigarette smoke-related disease
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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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Project description:Evaluation of mouse laryngeal inflammation upon low and high dose cigarette smoke exposures via NanoString analysis
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Project description:Cancer of the larynx is the second most common upper-aerodigestive cancer, and laryngeal squamous cell carcinoma (LSCC) is the major histological form. However, the molecular mechanism within LSCC progression remains poorly understood. MicroRNA-based target therapy is a promising approach in cancer therapy and offers multiple advantages as compared with the conventional treatment modalities. Hence, there is a need to identify the key microRNA involved in the progression of LSCC. We used GeneChip miRNA 2.0 array to profile the global microRNA deregulation in LSCC.
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Project description:Although smoking cessation shows clear cardiovascular risk benefits, lung-related disease risk remains higher in former smokers than in never smokers. To better understand the factors involved in this phenomenon, ApoE-/- mice were exposed to mainstream cigarette smoke (CS) or a smoking cessation-mimicking protocol for up to six months. Analysis of bronchoalveolar lavage fluid (BALF) from CS-exposed ApoE-/- mice revealed the presence of high concentrations of mediators involved in functions ranging from inflammation to cell proliferation and tissue remodeling. Gene expression levels for many analytes found elevated in BALF were also increased in lung tissue, indicating that the inflammatory response was the result of local tissue activation and the contribution of recruited inflammatory cells. Gene set enrichment analysis (GSEA) of expression data from lungs of CS-exposed mice showed activation of pathways involved in cell proliferation and tissue remodeling and a progressive deactivation upon smoke exposure cessation. Distinct activation patterns of inflammation, complement, and xenobiotic metabolism pathways were found in nasal epithelium and lung parenchyma during CS exposure and smoking cessation. Exposure of ApoE-/- mice to CS for up to 6 months induced adaptive and inflammatory responses in the respiratory tract that were partially deactivated upon cessation. We were able to reveal molecular perturbations accompanying these changes during CS exposure and cessation. Differential CS-mediated responses of pulmonary and nasal tissues reflect common mechanisms but also the varying degrees of epithelial functional specialization along the respiratory tract. These findings provide novel clues for the identification of markers of COPD progression.
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Project description:Exposure to cigarette smoke (CS) is etiologically linked to the development of fatal respiratory diseases, and there is a need to understand the mechanisms whereby CS causes damage. While animal models have provided valuable insights into smoking-related respiratory tract damage, modern toxicity testing calls for reliable in vitro models as alternatives for animal experimentation. Primary cells and immortalized cell lines can be used to gain some insight; however, the three-dimensional organotypic culture systems probably better mimic the morphological, physiological, and molecular attributes of the human respiratory tract. Even though the bronchus, bronchioles, and lung parenchyma are the primary sites of smoking-related respiratory disease manifestation, the nasal epithelium has been proposed as a surrogate tissue to study the effects of smoking on the respiratory tract. Here, we report on a repeated whole mainstream CS exposure of nasal and bronchial organotypic tissue cultures from which transcriptomic data were collected at several post-exposure time points. Despite the remarkably similar histology and cellular response to whole CS in both tissue types, as measured by cellular staining and cytokine secretion assessment, transcriptomic analyses combined with quantitative biological network modeling identified biological mechanisms that were unique to bronchial tissue at late post-exposure time points. Organotypic models therefore appear to be a promising alternative to animal experimentation, and provide species-relevant insights into the effects of CS exposure on the respiratory system.
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