期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 25, 期 1, 页码 13-26出版社
KARGER
DOI: 10.1159/000272047
关键词
Lung; Surfactant protein; Alveolar macrophages; Collectin; Receptor; Inflammation; Innate immunity
资金
- Juvenile Diabetes Researsch Foundation
- Potts Memorial Foundation
- University of Texas Health Science Center President's Council
- NIH/NHLBI Public Health grant [HL068127]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL068127] Funding Source: NIH RePORTER
Pulmonary surfactant has two crucial roles in respiratory function; first, as a biophysical entity it reduces surface tension at the air water interface, facilitating gas exchange and alveolar stability during breathing, and, second, as an innate component of the lung's immune system it helps maintain sterility and balance immune reactions in the distal airways. Pulmonary surfactant consists of 90% lipids and 10% protein. There are four surfactant proteins named SPA, SP-B, SP-C, and SP-D; their distinct interactions with surfactant phospholipids are necessary for the ultra-structural organization, stability, metabolism, and lowering of surface tension. In addition, SP-A and SP-D bind pathogens, inflict damage to microbial membranes, and regulate microbial phagocytosis and activation or deactivation of inflammatory responses by alveolar macrophages. SP-A and SP-D, also known as pulmonary collectins, mediate microbial phagocytosis via SP-A and SP-D receptors and the coordinated induction of other innate receptors. Several receptors (SP-R210, CD91/calreticulin, SIRP alpha, and toll-like receptors) mediate the immunological functions of SP-A and SP-D. However, accumulating evidence indicate that SP-B and SP-C and one or more lipid constituents of surfactant share similar immuno-regulatory properties as SP-A and SP-D. The present review discusses current knowledge on the interaction of surfactant with lung innate host defense. Copyright (C) 2010 S. Karger AG, Basel
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