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Acute Respiratory Distress Syndrome: Role of Oleic Acid-Triggered Lung Injury and Inflammation.

Gonçalves-de-Albuquerque CF, Silva AR, Burth P, Castro-Faria MV, Castro-Faria-Neto HC - Mediators Inflamm. (2015)

Bottom Line: One of the hallmarks of lung injury is edema formation with alveoli flooding.Animal models are used to study lung injury.The oleic acid has been linked to metabolic and inflammatory diseases; here we focus on lung injury.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz (FIOCRUZ), 21040-900 Rio de Janeiro, RJ, Brazil.

ABSTRACT
Lung injury especially acute respiratory distress syndrome (ARDS) can be triggered by diverse stimuli, including fatty acids and microbes. ARDS affects thousands of people worldwide each year, presenting high mortality rate and having an economic impact. One of the hallmarks of lung injury is edema formation with alveoli flooding. Animal models are used to study lung injury. Oleic acid-induced lung injury is a widely used model resembling the human disease. The oleic acid has been linked to metabolic and inflammatory diseases; here we focus on lung injury. Firstly, we briefly discuss ARDS and secondly we address the mechanisms by which oleic acid triggers lung injury and inflammation.

No MeSH data available.


Related in: MedlinePlus

Intracellular pathways activated in oleic acid-induced lung injury and inflammation. Oleic acid triggers intracellular pathways through different receptors ending up in inflammatory mediator production and/or cell death. MAPK: mitogen-activated protein kinases, ERK1/2: extracellular signal-regulated kinases, NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells, PI3K: phosphatidylinositol 3-kinase, AKT: protein kinase B, NLRC4: NLR family CARD domain-containing protein 4, MyD88: myeloid differentiation primary response gene 88, AP-1: activator protein 1, TLR: toll-like receptor, IL: interleukin, MIP: macrophage inflammatory protein, FFAR1: free fatty acid receptor 1, MCP1: monocyte chemotactic protein 1, TGFβ: transforming growth factor beta, and TNFα: tumor necrosis factor alpha.
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fig2: Intracellular pathways activated in oleic acid-induced lung injury and inflammation. Oleic acid triggers intracellular pathways through different receptors ending up in inflammatory mediator production and/or cell death. MAPK: mitogen-activated protein kinases, ERK1/2: extracellular signal-regulated kinases, NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells, PI3K: phosphatidylinositol 3-kinase, AKT: protein kinase B, NLRC4: NLR family CARD domain-containing protein 4, MyD88: myeloid differentiation primary response gene 88, AP-1: activator protein 1, TLR: toll-like receptor, IL: interleukin, MIP: macrophage inflammatory protein, FFAR1: free fatty acid receptor 1, MCP1: monocyte chemotactic protein 1, TGFβ: transforming growth factor beta, and TNFα: tumor necrosis factor alpha.

Mentions: The foremost target organ after oleic acid intravenous inoculation is the lungs, which retains about 85% of free fatty acids. The initial lesions occur as early as 5 min after administration [37] and last at least for 24 hours [38]. Oleic acid injected into the lung also induces neutrophil accumulation [36]. Increased TNFα and IL-8 levels after oleic acid injection [39], as well as IL-6, IL-1β, and the chemokine MIP-1α [36], were reported. Hence, oleic acid induces the synthesis of the main inflammatory mediators involved in clinical ARDS (Table 3 and Figures 1 and 2).


Acute Respiratory Distress Syndrome: Role of Oleic Acid-Triggered Lung Injury and Inflammation.

Gonçalves-de-Albuquerque CF, Silva AR, Burth P, Castro-Faria MV, Castro-Faria-Neto HC - Mediators Inflamm. (2015)

Intracellular pathways activated in oleic acid-induced lung injury and inflammation. Oleic acid triggers intracellular pathways through different receptors ending up in inflammatory mediator production and/or cell death. MAPK: mitogen-activated protein kinases, ERK1/2: extracellular signal-regulated kinases, NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells, PI3K: phosphatidylinositol 3-kinase, AKT: protein kinase B, NLRC4: NLR family CARD domain-containing protein 4, MyD88: myeloid differentiation primary response gene 88, AP-1: activator protein 1, TLR: toll-like receptor, IL: interleukin, MIP: macrophage inflammatory protein, FFAR1: free fatty acid receptor 1, MCP1: monocyte chemotactic protein 1, TGFβ: transforming growth factor beta, and TNFα: tumor necrosis factor alpha.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4660020&req=5

fig2: Intracellular pathways activated in oleic acid-induced lung injury and inflammation. Oleic acid triggers intracellular pathways through different receptors ending up in inflammatory mediator production and/or cell death. MAPK: mitogen-activated protein kinases, ERK1/2: extracellular signal-regulated kinases, NFκB: nuclear factor kappa-light-chain-enhancer of activated B cells, PI3K: phosphatidylinositol 3-kinase, AKT: protein kinase B, NLRC4: NLR family CARD domain-containing protein 4, MyD88: myeloid differentiation primary response gene 88, AP-1: activator protein 1, TLR: toll-like receptor, IL: interleukin, MIP: macrophage inflammatory protein, FFAR1: free fatty acid receptor 1, MCP1: monocyte chemotactic protein 1, TGFβ: transforming growth factor beta, and TNFα: tumor necrosis factor alpha.
Mentions: The foremost target organ after oleic acid intravenous inoculation is the lungs, which retains about 85% of free fatty acids. The initial lesions occur as early as 5 min after administration [37] and last at least for 24 hours [38]. Oleic acid injected into the lung also induces neutrophil accumulation [36]. Increased TNFα and IL-8 levels after oleic acid injection [39], as well as IL-6, IL-1β, and the chemokine MIP-1α [36], were reported. Hence, oleic acid induces the synthesis of the main inflammatory mediators involved in clinical ARDS (Table 3 and Figures 1 and 2).

Bottom Line: One of the hallmarks of lung injury is edema formation with alveoli flooding.Animal models are used to study lung injury.The oleic acid has been linked to metabolic and inflammatory diseases; here we focus on lung injury.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz (FIOCRUZ), 21040-900 Rio de Janeiro, RJ, Brazil.

ABSTRACT
Lung injury especially acute respiratory distress syndrome (ARDS) can be triggered by diverse stimuli, including fatty acids and microbes. ARDS affects thousands of people worldwide each year, presenting high mortality rate and having an economic impact. One of the hallmarks of lung injury is edema formation with alveoli flooding. Animal models are used to study lung injury. Oleic acid-induced lung injury is a widely used model resembling the human disease. The oleic acid has been linked to metabolic and inflammatory diseases; here we focus on lung injury. Firstly, we briefly discuss ARDS and secondly we address the mechanisms by which oleic acid triggers lung injury and inflammation.

No MeSH data available.


Related in: MedlinePlus