期刊
ANNUAL REVIEW OF PHYSIOLOGY, VOL 76
卷 76, 期 -, 页码 467-492出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021113-170408
关键词
efferocytosis; proresolving mediators; polyunsaturated fatty acid; lipoxin; resolvin; protectin; maresin; asthma; acute respiratory distress syndrome; pneumonia; catabasis
类别
资金
- NHLBI NIH HHS [P50 HL107166, U01 HL108712, U10HL108712, U10 HL109172, P50HL107116, U10HL109172, R01 HL068669, HL068669, R01 HL122531] Funding Source: Medline
- NIGMS NIH HHS [P01 GM095467] Funding Source: Medline
- PHS HHS [P01MG0095467] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL122531, U01HL108712, P50HL107166, R01HL068669, U10HL109172] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P01GM095467] Funding Source: NIH RePORTER
Acute inflammation in the lung is essential to health. So too is its resolution. In response to invading microbes, noxious stimuli, or tissue injury, an acute inflammatory response is mounted to protect the host. To limit inflammation and prevent collateral injury of healthy, uninvolved tissue, the lung orchestrates the formation of specialized proresolving mediators, specifically lipoxins, resolvins, protectins, and maresins. These immunoresolvents are agonists for resolution that interact with specific receptors on leukocytes and structural cells to blunt further inflammation and promote catabasis. This process appears to be defective in several common lung diseases that are characterized by excess or chronic inflammation. Here, we review the molecular and cellular effectors of resolution of acute inflammation in the lung.
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