Role of heparin in pulmonary cell populations in an in-vitro model of acute lung injuryReportar como inadecuado




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Respiratory Research

, 18:89

First Online: 10 May 2017Received: 28 December 2016Accepted: 03 May 2017DOI: 10.1186-s12931-017-0572-3

Cite this article as: Camprubí–Rimblas, M., Guillamat-Prats, R., Lebouvier, T. et al. Respir Res 2017 18: 89. doi:10.1186-s12931-017-0572-3

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.

KeywordsAcute Respiratory Distress Syndrome ARDS Alveolar macrophages Alveolar cells Fibroblasts Anticoagulants Inflammation AbbreviationsALIAcute lung injury

ARDSAcute respiratory distress syndrome

BALBroncho-alveolar lavage

FBSFetal bovine solution

hAMHuman alveolar macrophages

hATIIAlveolar type II cells

HBSSHanks Balanced Salt solution

hFFibroblasts

LPSLipopolysaccharide from Escherichia coli 055:B5

UFHUnfractionated heparin





Autor: Marta Camprubí–Rimblas - Raquel Guillamat-Prats - Thomas Lebouvier - Josep Bringué - Laura Chimenti - Manuela Iglesias -

Fuente: https://link.springer.com/







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