A cost-effective technique for generating preservable biomass smoke extract and measuring its effect on cell receptor expression in human bronchial epithelial cells.

Nearly half of the world's population uses biomass fuel for the purposes of cooking and heating. Smoke derived from biomass increases the risk of the development of lung diseases, including pneumonia, chronic obstructive pulmonary disease, airway tract infections, and lung cancer. Despite the evidence linking biomass smoke exposure to pulmonary disease, only a small number of experimental studies have been conducted on the impact of biomass smoke on airway epithelial cells. This is in part due to the lack of a standard and easily accessible procedure for the preparation of biomass smoke. Here, we describe a cost-effective and reproducible method for the generation of different smoke extracts, in particular, cow dung smoke extract (CDSE) and wood smoke extract (WSE) for use in a range of biological applications. We examined the effect of the biomass smoke extracts on human bronchial epithelial cell expression of a known responder to cigarette smoke exposure (CSE), the platelet-activating factor receptor (PAFR). Similar to the treatment with CSE, we observed a dose-dependent increase in PAFR expression on human airway epithelial cells that were exposed to CDSE and WSE. This method provides biomass smoke in a re-usable form for cell and molecular bioscience studies on the pathogenesis of chronic lung disease

Effects of chemical composition on the lung cell response to coal particles: Implications for coal workers' pneumoconiosis

Background and objectiveCoal mine dust has a complex and heterogeneous chemical composition. It has been suggested that coal particle chemistry plays a critical role in determining the pathogenesis of coal workers' pneumoconiosis (CWP). In this study, we aimed to establish the association between the detrimental cellular response and the chemical composition of coal particles. MethodsWe sourced 19 real-world coal samples. Samples were crushed prior to use to minimize the impact of particle size on the response and to ensure the particles were respirable. Key chemical components and inorganic compounds were quantified in the coal samples. The cytotoxic, inflammatory and pro-fibrotic responses in epithelial cells, macrophages and fibroblasts were assessed following 24 h of exposure to coal particles. Principal component analysis (PCA) and stepwise regression were used to determine which chemical components of the coal particles were associated with the cell response. ResultsThe cytotoxic, inflammatory and pro-fibrotic response varied considerably between coal samples. There was a high level of collinearity in the cell responses and between the chemical compounds within the coal samples. PCA identified three factors that explained 75% of the variance in the cell response. Stepwise multiple regression analysis identified K2O (p 2O3 (p = 0.011) as significant predictors of cytotoxicity and cytokine production, respectively. ConclusionOur data clearly demonstrate that the detrimental cellular effects of exposure to coal mine dusts are highly dependent on particle chemistry. This has implications for understanding the pathogenesis of CWP

A cost-effective technique for generating preservable biomass smoke extract and measuring its effect on cell receptor expression in human bronchial epithelial cells

Nearly half of the world’s population uses biomass fuel for the purposes of cooking and heating. Smoke derived from biomassincreases the risk of the development of lung diseases, including pneumonia, chronic obstructive pulmonary disease,airway tract infections, and lung cancer. Despite the evidence linking biomass smoke exposure to pulmonary disease, onlya small number of experimental studies have been conducted on the impact of biomass smoke on airway epithelial cells.This is in part due to the lack of a standard and easily accessible procedure for the preparation of biomass smoke. Here, wedescribe a cost-effective and reproducible method for the generation of different smoke extracts, in particular, cow dungsmoke extract (CDSE) and wood smoke extract (WSE) for use in a range of biological applications. We examined the effect ofthe biomass smoke extracts on human bronchial epithelial cell expression of a known responder to cigarette smoke exposure(CSE), the platelet-activating factor receptor (PAFR). Similar to the treatment with CSE, we observed a dose-dependentincrease in PAFR expression on human airway epithelial cells that were exposed to CDSE and WSE. This method providesbiomass smoke in a re-usable form for cell and molecular bioscience studies on the pathogenesis of chronic lung disease

A cost-effective technique for generating preservable biomass smoke extract and measuring its effect on cell receptor expression in human bronchial epithelial cells

Nearly half of the world’s population uses biomass fuel for the purposes of cooking and heating. Smoke derived from biomassincreases the risk of the development of lung diseases, including pneumonia, chronic obstructive pulmonary disease,airway tract infections, and lung cancer. Despite the evidence linking biomass smoke exposure to pulmonary disease, onlya small number of experimental studies have been conducted on the impact of biomass smoke on airway epithelial cells.This is in part due to the lack of a standard and easily accessible procedure for the preparation of biomass smoke. Here, wedescribe a cost-effective and reproducible method for the generation of different smoke extracts, in particular, cow dungsmoke extract (CDSE) and wood smoke extract (WSE) for use in a range of biological applications. We examined the effect ofthe biomass smoke extracts on human bronchial epithelial cell expression of a known responder to cigarette smoke exposure(CSE), the platelet-activating factor receptor (PAFR). Similar to the treatment with CSE, we observed a dose-dependentincrease in PAFR expression on human airway epithelial cells that were exposed to CDSE and WSE. This method providesbiomass smoke in a re-usable form for cell and molecular bioscience studies on the pathogenesis of chronic lung disease