Abstract
BackgroundIn the early stages of acute respiratory distress syndrome (ARDS), pro-inflammatory mediators inhibit natural anticoagulant factors and initiate an increase in procoagulant activity. Previous studies proved the beneficial effects of heparin in pulmonary coagulopathy, which derive from its anticoagulant and anti-inflammatory activities, although it is uncertain whether heparin works. Understanding the specific effect of unfractioned heparin on cell lung populations would be of interest to increase our knowledge about heparin pathways and to treat ARDS.MethodsIn the current study, the effect of heparin was assessed in primary human alveolar macrophages (hAM), alveolar type II cells (hATII), and fibroblasts (hF) that had been injured with LPS.ResultsHeparin did not produce any changes in the Smad/TGFß pathway, in any of the cell types evaluated. Heparin reduced the expression of pro-inflammatory markers (TNF-α and IL-6) in hAM and deactivated the NF-kß pathway in hATII, diminishing the expression of IRAK1 and MyD88 and their effectors, IL-6, MCP-1 and IL-8.ConclusionsThe current study demonstrated that heparin significantly ameliorated the cells lung injury induced by LPS through the inhibition of pro-inflammatory cytokine expression in macrophages and the NF-kß pathway in alveolar cells. Our results suggested that a local pulmonary administration of heparin through nebulization may be able to reduce inflammation in the lung; however, further studies are needed to confirm this hypothesis.
Highlights
In the early stages of acute respiratory distress syndrome (ARDS), pro-inflammatory mediators inhibit natural anticoagulant factors and initiate an increase in procoagulant activity
Acute respiratory distress syndrome (ARDS) is a common and devastating illness characterized by lung inflammation, endothelial and epithelial injury, increased vascular permeability and oedema; all of these factors lead to organ dysfunction
The objective of this study was to test the effect of Unfractionated heparin (UFH), in inflammation–proliferation–permeabilisation in various primary lung cells such as human alveolar macrophages, human alveolar type II cells, and human fibroblasts in vitro after lipopolysaccharide (LPS)-induced acute injury
Summary
In the early stages of acute respiratory distress syndrome (ARDS), pro-inflammatory mediators inhibit natural anticoagulant factors and initiate an increase in procoagulant activity. Acute respiratory distress syndrome (ARDS) is a common and devastating illness characterized by lung inflammation, endothelial and epithelial injury, increased vascular permeability and oedema; all of these factors lead to organ dysfunction. Pulmonary coagulopathy is intrinsic to ARDS and directly dependent on the severity of acute lung injury (ALI) and linked to the outcome of ARDS. This disease is characterized by the coagulation cascade activation and reduced fibrinolysis that leads to fibrin deposition in the airspaces and triggers inflammation. All of this occurs because of the alveolar type II cell damage and the pro-inflammatory activation of macrophages
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