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Eicosapentaenoic acid reduces pulmonary endothelial cell adhesion protein expression with IL-6
Critical Care Medicine ; 50(1 SUPPL):539, 2022.
Artigo em Inglês | EMBASE | ID: covidwho-1691827
ABSTRACT

INTRODUCTION:

Infectious agents, including SARSCoV- 2, cause pulmonary endothelial cell (EC) dysfunction that leads to acute respiratory distress syndrome (ARDS). EC dysfunction involves increased leukocyte recruitment and cell permeability mediated by various junctional proteins, integrins, and adhesion molecules. The omega-3 fatty acid eicosapentaenoic acid (EPA) and its metabolites modulate inflammation and vascular function. These actions of EPA may contribute to reduced cardiovascular events as reported in outcome trials such as REDUCE-IT. Currently, EPA is being tested in patients at risk for or with COVID-19. This study tested the effects of EPA on protein expression in human pulmonary ECs following challenge by the cytokine IL-6 to simulate conditions encountered in advanced viral infections.

METHODS:

Human lung microvascular endothelial cells (HMVEC-L) were post-treated with vehicle or EPA (40 μM) in 2% FBS after a 2 hr challenge with IL-6 at 12 ng/ml for 24 h. Proteomic analysis used LC/MS to assess relative expression levels of EC proteins. Only significant (p< 0.05) changes in protein expression between treatment groups >1-fold were analyzed. Specific pathway analysis was carried out using gene set enrichment analysis (GSEA).

RESULTS:

HMVEC-L treated with EPA following challenge with IL-6 showed significant changes in over 400 proteins compared with IL-6 treatment alone. EPA specifically diminished eleven proteins in the “integrin cell surface interactions” pathway. These pathways proteins included integrins alpha-V, alpha-6, and beta-1, along with PECAM-1, junction adhesion molecule C (JAM3), fibronectin, and ICAM- 2.

CONCLUSIONS:

EPA reduced expression of pulmonary endothelial adhesion and permeability proteins following IL-6 treatment. The ability of EPA to inhibit EC dysfunction and inflammation may have benefits for patients with or at risk for ARDS due to viruses such as SARS-CoV-2 or sepsis.
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Texto completo: Disponível Coleções: Bases de dados de organismos internacionais Base de dados: EMBASE Idioma: Inglês Revista: Critical Care Medicine Ano de publicação: 2022 Tipo de documento: Artigo

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Texto completo: Disponível Coleções: Bases de dados de organismos internacionais Base de dados: EMBASE Idioma: Inglês Revista: Critical Care Medicine Ano de publicação: 2022 Tipo de documento: Artigo