Anthracosis is an injury to the lung epithelial tissue and the tracheobronchial tree, which can be caused by the deposition of particles of air pollution, and usually leads to respiratory complications due to the initial inflammation leading to the installation of fibrosis due to inadequate repair of respiratory tissues. One of the mechanisms that occur in the respiratory tract cell is the biotransformation of the xenobiotics that are adsorbed to the particles of air pollution through specific biochemical reactions, with the performance of ordered enzymes. The coding of these enzymes that aid in the excretion of xenobiotic compounds is performed by the CYP gene superfamily, with CYP1A1 being the main enzyme found in the respiratory epithelium responsible for the metabolism of xenobiotics. For the studies of the effects of certain cells on particle exposure, a co-culture of two cell types (epithelial and inflammatory) is proposed to evaluate relevant aspects of this interaction with the aim of studying the expression of the CYP1A1 gene in co-culture of BEAS-2B cells and macrophages (M1 or M2), when exposed to particulate matter collected from air pollution (PM2.5) and anthracosis collected from cadaver of the USP Capital Deaths Checking Service (SVO), relating the outcomes with the pathophysiology of anthracosis.
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