Abstract
Clinical acute lung injury (ALI) is a major cause of acute respiratory failure in critically ill patients. There is considerable experimental and clinical evidence that pro- and anti-inflammatory cytokines play a major role in the pathogenesis of inflammatory-induced lung injury from sepsis, pneumonia, aspiration, and shock. A recent multi-center clinical trial found that a lung-protective ventilatory strategy reduces mortality by 22% in patients with ALI. Interestingly, this protective ventilatory strategy was associated with a marked reduction in the number of neutrophils and the concentration of pro-inflammatory cytokines released into the airspaces of the injured lung. Further research is needed to establish the contribution of cytokines to both the pathogenesis and resolution of ALI.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Chemokines / metabolism
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Chemotactic Factors / metabolism
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Clinical Trials as Topic
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Cytokines / biosynthesis*
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Cytokines / metabolism
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Edema / immunology
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Enzyme-Linked Immunosorbent Assay
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HMGB1 Protein / metabolism
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Humans
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Inflammation / metabolism*
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Interleukin-1 / metabolism
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Interleukin-10 / metabolism
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Interleukin-8 / immunology
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Ligands
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Lung / immunology
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Lung Injury*
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Macrophage Migration-Inhibitory Factors / metabolism
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Models, Biological
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Multicenter Studies as Topic
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Neutrophils / metabolism
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Respiratory Distress Syndrome / immunology*
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Respiratory Distress Syndrome / metabolism
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Time Factors
Substances
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Chemokines
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Chemotactic Factors
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Cytokines
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HMGB1 Protein
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Interleukin-1
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Interleukin-8
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Ligands
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Macrophage Migration-Inhibitory Factors
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Interleukin-10