Anti - IL17 treatment control responses in lung injury induced by elastase

Aims: IL17 may be the target for treatment of pulmonary diseases. Objectives: To evaluate effects of anti-IL17 in a model of lung injury induced by elastase. Methods: we studied respiratory system resistance (Rrs), respiratory system elastance (Ers), airway resistance (Raw), pulmonary parenchyma resistance (Gtis), pulmonary parenchyma elastance (Htis), exhaled nitric oxide (NOex), total cell count of bronchoalveolar lavage fluid (FLBA), positive cells for MMP9, MMP12, INOS, NFkb, IL17, collagen and elastic fibers in airways and alveolar septa, and mean linear intercept (Lm) in 32 male C57Bl6 mice divided into four groups: SAL(intratracheal (IT) and intraperithoneal (IP) saline); EC(IP saline and IT elastase); EP(anti-IL17 IP 3 hours before elastase IT); ET(anti-IL17 IP on days 25, 26, 27 and 28 post elastase). Results: There was increase on Rrs, Ers, Raw, Htis, NOex and FLBA in EC compared to SAL (p<0,05). In EP and ET, Rrs, Ers, Raw, Htis and NOex decreased, compared to the EC (p<0.05). There was reduction in FLBA in ET compared to the EC and EP (p<0.05). There was no difference between EC and EP. The positive cells for NFkb, iNOS, MMP9, MMP12, IL17 were reduced in airways and alveolar septa in EP and ET when compared to EC and volume fraction of collagen fibers in airways and elastic fibers in alveolar septa (p<0.05). Lm was increased in EC compared to SAL and treatment with anti-IL17 decreased these values in EP and ET (p<0.05). Conclusions: Anti-IL17 contributed to improve lung mechanics, inflammation, remodelling of the extracellular matrix and the response to oxidative stress in alveolar septa and airway walls in this model of lung injury. Financial Support: Capes, FAPESP, CNPq, LIM-20-HC-FMUSP.