急性呼吸窘迫综合征
细胞因子
免疫学
医学
肺
炎症
促炎细胞因子
细胞生物学
发病机制
生物
内科学
出处
期刊:Chest
[Elsevier]
日期:1999-07-01
卷期号:116: 2S-8S
被引量:134
标识
DOI:10.1378/chest.116.suppl_1.2s
摘要
The cellular and molecular basis for ARDS remains uncertain > 30 years after the original description of the syndrome. With the explosion of information about the involvement of cells and cytokines in inflammation, there has been intense interest in understanding the involvement of cytokines in the pathogenesis of ARDS. Cytokines are low-molecular-weight soluble proteins (generally < 30 kda) that transmit signals between cells. It is now clear that cytokine production is not limited to lymphoid and myeloid cells, and that cytokines produced by epithelial and mesenchymal cells amplify inflammatory responses in the lungs and other organs. Cytokines are produced in “cascades” in which the initial cytokine signals are amplified many-fold by target cells, such as epithelial cells, fibroblasts, and endothelial cells. Cytokines function in “networks” in which feedback occurs at many points to coordinate and regulate cytokine and cellular responses.
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