Inflammatory Cytokines in the BAL of Patients With ARDS

Meduri, G. Umberto; Kohler, Gary; Headley, Stacey; Tolley, Elizabeth A.; Stentz, Frankie B.; Postlethwaite, Arnold E.

doi:10.1378/chest.108.5.1303

Cited by 612 publications

(150 citation statements)

References 59 publications

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“…7), and TNF-␣, neutrophil infiltration, the mouse interleukin-8 equivalent, KC, and MIP-2 were measured in the recovered lavage fluid (44). These inflammatory mediators are important prognostic determinants of ALI/ARDS in humans (45). LPS-induced TNF-␣ was ϳ300 pg/ml and was unaffected by DPPC instillation.…”

Section: Popg Inhibits the Lps-induced Phosphorylation Of Mapk And Ibmentioning

confidence: 95%

Anionic Pulmonary Surfactant Phospholipids Inhibit Inflammatory Responses from Alveolar Macrophages and U937 Cells by Binding the Lipopolysaccharide-interacting Proteins CD14 and MD-2

Kuronuma¹,

Mitsuzawa²,

Takeda

et al. 2009

Journal of Biological Chemistry

135

203

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Lipopolysaccharide (LPS), derived from Gram-negative bacteria, is a major cause of acute lung injury and respiratory distress syndrome. Pulmonary surfactant is secreted as a complex mixture of lipids and proteins onto the alveolar surface of the lung. Surfactant phospholipids are essential in reducing surface tension at the air-liquid interface and preventing alveolar collapse at the end of the respiratory cycle. In the present study, we determined that palmitoyl-oleoyl-phosphatidylglycerol and phosphatidylinositol, which are minor components of pulmonary surfactant, and synthetic dimyristoylphosphatidylglycerol regulated the inflammatory response of alveolar macrophages. The anionic lipids significantly inhibited LPS-induced nitric oxide and tumor necrosis factor-␣ production from rat and human alveolar macrophages and a U937 cell line by reducing the LPS-elicited phosphorylation of multiple intracellular protein kinases. The anionic lipids were also effective at attenuating inflammation when administered intratracheally to mice challenged with LPS. Binding studies revealed high affinity interactions between the palmitoyl-oleoylphosphatidylglycerol and the Toll-like receptor 4-interacting proteins CD14 and MD-2. Our data clearly identify important antiinflammatory properties of the minor surfactant phospholipids at the environmental interface of the lung.

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Section: Popg Inhibits the Lps-induced Phosphorylation Of Mapk And Ibmentioning

confidence: 95%

Anionic Pulmonary Surfactant Phospholipids Inhibit Inflammatory Responses from Alveolar Macrophages and U937 Cells by Binding the Lipopolysaccharide-interacting Proteins CD14 and MD-2

Kuronuma¹,

Mitsuzawa²,

Takeda

et al. 2009

Journal of Biological Chemistry

135

203

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“…Although no studies to date have addressed whether mechanical ventilation per se is capable of altering lung cellular function leading to production of inflammatory mediators and lung injury, there is some evidence in the literature to support the plausibility of this postulate. Clinical studies of patients developing ARDS have noted an association between lung inflammatory mediators and the development of physiologic abnormalities (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model.

Tremblay¹,

Valenza²,

Ribeiro³

et al. 1997

J. Clin. Invest.

1,212

754

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“…In regard to these questions, Donnelly et al (68) recently reported the presence of the migration inhibitory factor produced by macrophages in BAL fluids, which favours the production of proinflammatory cytokines and inhibits the anti-inflammatory action of corticosteroids. The presence of sustained increased levels of these proinflammatory cytokines in fatal ARDS was indeed emphasized by Meduri et al (69). In keeping with this observation of an altered balance between proinflammatory and anti-inflammatory cytokines in ARDS, Donnelly et al (64) observed that low concentrations of anti-inflammatory cytokines such as IL-10 were linked closely to a poor prognosis.…”

Section: Inflammation and Neutrophils In Ardsmentioning

confidence: 78%

“…There have been proposals to use granulocytecolony-stimulating factor (G-CSF) in infected non-neutropenic patients to improve organ recovery, prevent ARDS and increase survival (69). G-CSF dramatically enhances neutrophil recruitment and targets their defence capabilities to damaged organs, clearing debris and restoring function (69).…”

Section: Inflammation and Neutrophils In Ardsmentioning

confidence: 99%

Acute Respiratory Distress Syndrome: 30 Years Later?

Lesur¹,

Berthiaume

Blaise

et al. 1999

Canadian Respiratory Journal

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Acute respiratory distress syndrome (ARDS) was first described about 30 years ago. Modern definitions and statements have recently been proposed to describe ARDS accurately, but none is perfect. Diffuse alveolar damage is the basic pathological pattern most commonly observed in ARDS, and the term includes permeability edema. The alveolar epithelium of the alveolar-capillary barrier is clearly a key component requiring repair, given its multipotent functional activity. Lung inflammation and neutrophil accumulation are essential markers of disease in ARDS, and a wide variety of pro- and anti-inflammatory cytokines have been described in the alveolar fluid and blood of patients. These molecules still have to prove their value as diagnostic or prognostic biomarkers of ARDS.Supportive therapy in ARDS improved in the past decade; mechanical ventilation with lung protective strategies and patient positioning are gaining interest, but the indications for corticosteroids for ARDS are still debated. Nitric oxide may have a place in the treatment of one-third of patients. Novel approaches, such as surfactant replacement and liquid ventilation, may further improve supportive therapy. Innovative interventions may be on the horizon in treatments that help to resolve or modulate common pathways of ARDS, such as inflammation (eg, granulocyte-colony stimulating factor) or epithelial repair (eg, keratinocyte growth factor).

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Inflammatory Cytokines in the BAL of Patients With ARDS

Cited by 612 publications

References 59 publications

Anionic Pulmonary Surfactant Phospholipids Inhibit Inflammatory Responses from Alveolar Macrophages and U937 Cells by Binding the Lipopolysaccharide-interacting Proteins CD14 and MD-2

Anionic Pulmonary Surfactant Phospholipids Inhibit Inflammatory Responses from Alveolar Macrophages and U937 Cells by Binding the Lipopolysaccharide-interacting Proteins CD14 and MD-2

Injurious ventilatory strategies increase cytokines and c-fos m-RNA expression in an isolated rat lung model.

Acute Respiratory Distress Syndrome: 30 Years Later?

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