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Gluthathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells
Citation:
Wu, W., D. Peden, R. McConnell, S. Fruin, AND D. Diaz-Sanchez. Gluthathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells. Particle and Fibre Toxicology. BioMed Central Ltd, London, Uk, 9(31):doi:1186/1743-8977, (2012).
Impact/Purpose:
Diesel exhaust particles (DEP) emitted during the combustion of diesel fuel are an important contributor to the levels of particulate matter (PM) air pollution in urban areas. These particles comprise a carbonaceous core to which organic and inorganic compounds, such as polycyclic aromatic hydrocarbons (PAHs), nitro and oxygenated derivatives of PAHs, heterocyclic compounds, aldehydes, aliphatic hydrocarbons, and heavy metals, can be adsorbed. Epidemiological and experimental studies have shown that DEP inhalation is associated with elevated incidence of diverse respiratory disorders including pulmonary inflammation, increased susceptibility to respiratory infections, increased risk of lung cancer, and exacerbation of asthma and chronic obstructive pulmonary diseases [1—4]. However, the mechanisms underlying DEP-induced pulmonary disorders have not yet been adequately elucidated.
Description:
Diesel exhaust particles (DEP) contribute substantially to ambient particulate matter (PM) air pollution in urban areas. Inhalation of PM has been associated with increased incidence of lung disease in susceptible populations. We have demonstrated that the glutathione-S-transferase M1 (GSTM1) null genotype could aggravate DEP-induced airway inflammation in human subjects. Given the critical role airway epithelial cells play in the pathogenesis of airway inflammation, we established the GSTM1 deficiency condition in primary bronchial epithelial cells from human volunteers with GSTM1 sufficient genotype (GSTM1+) using GSTM1 shRNA to determine whether GSTM1 deficiency could exaggerate DEP-induced expression of interleukin-8 (IL-8) and IL-1B proteins. Furthermore, the mechanisms underlying GSTM 1 regulation of DEP-induced IL-8 and IL-1B expression were also investigated.