Silicosis is on the rise, but is there a therapeutic target ?

© David Gosset / P@CYFIC facility / CBM / CNRS   Dendritic cell (a type of immun
© David Gosset / P@CYFIC facility / CBM / CNRS Dendritic cell (a type of immune cell) in a state of stress following silica exposure. Signs of cell stress are (i) the presence of DNA (shown in blue)—which is normally confined to the nucleus and mitochondria—within the cytoplasm and outside of the cell and (ii) activation of the STING pathway accompanied by the formation of punctae (shown in red). Silica crystals engulfed by the cell are visible as translucent grains in the image on the right.
Paris, 6 December 2018 Researchers from the CNRS, the University of Orléans, and the company Artimmune, in collaboration with Turkish clinicians from Atatürk University, have identified a key mechanism of lung inflammation induced by silica exposure, which leads to silicosis, an incurable disease. Their study in mice and patients, published (December 6th, 2018), shows that this inflammation can be prevented by extracellular DNA degradation, suggesting a new therapeutic target. Provoked by silica inhalation, silicosis is a fatal disease, the only cure being lung transplantation. Though known as a miner's disease, it is far from a relic of the past : new operations using high-pressure sand—like denim sandblasting and fracking in shale gas extraction—expose workers and neighbor residents. Worldwide, silicosis still affects tens of millions of people, especially those active in the construction and mining industries, but also textile and dentistry professionals. Once in the airways, silica microparticles provoke cell stress and death, and finally, chronic inflammation and fibrosis (replacement of normal lung tissue with scar tissue). This leads to an irreversible reduction in respiratory capacity as silica is not eliminated.
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