Heparin effect in pulmonary cell populations in an in-vitro model of acute lung injury

Acute Lung Injury(ALI) inflammation is initiated by alveolar macrophages(AM) which release proinflammatory mediators highly regulated for other pulmonary cells. Coagulation pathways are involved in the injury progress. The beneficial effect of anticoagulants is due to their anti-inflammatory effect and their anticoagulant activity. Objective: Evaluate the specific effect of heparin in different pulmonary cells after ALI induction. Human alveolar type II cells(ATII), AM and fibroblasts were isolated from pulmonary biopsies. Heparin (0,1IU/ml) was administered to the cells after the induction of an ALI with a pro-inflammatory stimulus with Lipopolysaccharide from E. coli 055:B5(LPS). The effect of heparin was assessed by the analysis of pro and anti-inflammatory markers and their pathways via qRT-PCR. Data are expressed as mean±SEM. Statistical analysis was performed using One-Way-ANOVA and Newman-Keuls post-hoc test. Statistical significance p≤0.05 is considered. Results: Heparin was able to modify the inflammatory response of all cell populations via NFkB pathway, decreasing it significantly in the case of ATII. Heparin did not produce any changes in the SMAD/TGFβ pathway. Conclusions: Heparin has an immunomodulatory effect in alveolar cells and reduces inflammation in ATII and macrophages. To go in deep in heparin interaction with pulmonary cells promote the development of specific treatments for ALI.