Industrial development has been characterized by the introduction of a number of synthetically produced chemical compounds that have led to an ever-greater increase of novel substances released into the environment and potentially capable of affecting human health. These chemicals can enter the human body through various routes such as food consumption, breathing or adsorption. Since the immune system senses and reacts to any xenobiotic, growing attention has been paid to the role that environmental pollutants can play in the perturbation of immunological activities. Despite the fact that several families of brominated flame-retardants (FRs) have been listed as POPs and thus banned from production, several papers have reported the persistent presence of this class of chemicals in the environment and in animal and human tissues, suggesting a risk for human health. Immune cells have been shown to recognize and respond to xenobiotics in different ways depending on several mechanisms including the release of diverse arrays of soluble factors (i.e. cytokines and chemokines), through epigenetic modifications (i.e. the modulation of the expression of microRNAs) and the secretion of extracellular vesicles and modification of their cargo content for communication to distant cells and organs. Our data suggest that a flame-retardant such as the PBDE-47 is capable of perturbing the expression of macrophage pro-inflammatory cytokines and genes involved in cell motility affecting macrophage performance. Indeed, PBDE-47 is capable of modulating the macrophage intracellular miRNA profile and the biogenesis as well as the cargo content of macrophage-derived sEVs, exacerbating the expression of genes involved in the LPS induced inflammatory response in naïve macrophages.


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