Synthetic surfactant (Exosurf) inhibits endotoxin-stimulated cytokine secretion by human alveolar macrophages.
Synthetic surfactant (Exosurf) inhibits endotoxin-stimulated cytokine secretion by human alveolar macrophages.
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合成表面活性剂 (Exosurf) 抑制人肺泡巨噬细胞内毒素刺激的细胞因子分泌。
DOI:
10.1165/ajrcmb/7.3.257
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发表时间:
1992
影响因子:
6.4
通讯作者:
Wiedemann,HP
中科院分区:
文献类型:
--
作者:
Thomassen,MJ;Meeker,DP;Antal,JM;Connors,MJ;Wiedemann,HP
Tumor necrosis factor-a (TNF), interleukin-l, 8 (IL-l), interleukin-6 (IL-6), and interleukin-8 (IL-8) are inflammatory cytokines produced by alveolar macrophages (AMs) and implicated in sepsis-related adult respiratory distress syndrome (ARDS). Preliminary findings from clinical trials suggest that aerosolized delivery of the synthetic surfactant Exosurf (Burroughs Wellcome Co.) reduces mortality in patients with sepsis-induced ARDS. The purpose of the present study was to examine the effectof Exosurf on inflammatory cytokine secretion from AMs in vitro. AMs were obtained from normal nonsmoking adult volunteers. Secreted TNF, IL-l, IL-6, and IL-8 were measured by enzyme-linked immunoassays in 24 h culture fluids of AMs. Exosurf inhibited LPS-stimulated TNF, IL-l, and IL-6 secretion in a dose-dependent fashion. IL-8 secretion was not affected by Exosurf under these conditions. However, if AMs were preincubated for 24 h in media and then LPS-stimulated, IL-8 secretion was inhibited by Exosurf. Regulation of IL-8 production may differ from TNF, IL-l, and IL-6. Unstimulated cytokine secretion was not affected by any of the tested concentrations of Exosurf. The inhibitory effect of Exosurf on endotoxin-induced cytokine secretion by human AMs suggeststhat Exosurf may modulate inflammatory cytokine production in the lung.Surfactant replacement therapy in neonatal respiratory distress syndrome reduces morbidity and mortality (1-4). Recent preliminary studies with the synthetic surfactant Exosurf have also shown an apparent trend toward reduction in the mortality associated with sepsis-related adult respiratory distress syndrome (ARDS)(5). Inflammatory cytokines such as tumor necrosis factor-a (TNF), interleukin-l, 8 (IL-l), and interleukin-6 (IL-6) have been implicated in the pathogenesis of sepsis and ARDS (6-13). Since the neutrophil plays a prominent role in the development of ARDS (14), interleukin-8 (IL-8; neutrophil chemotactic factor) has also been implicated. A previous study demonstrated that lipopolysaccharide (LPS)-stimulated monocyte TNF secretion is
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DOI:
--
发表时间:
1987
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Fuhlbrigge,RC;Chaplin,DD;Kiely,JM;Unanue,ER
通讯作者:
Unanue,ER
DOI:
--
发表时间:
1991
期刊:
影响因子:
--
作者:
W. Long;A. Corbet;R. Cotton;S. Courtney;G. McGuiness;D. Walter;J. Watts;J. Smyth;H. Bard;V. Chernick
通讯作者:
V. Chernick
影响因子:
3.6
作者:
M. Thomassen;B. Boxerbaum;C. Demko;Paula J Kuchenbrod;D. Dearborn;R. Wood
通讯作者:
R. Wood
DOI:
--
发表时间:
1986
期刊:
The American journal of pathology
影响因子:
--
作者:
Bachwich,PR;Lynch3rd,JP;Larrick,J;Spengler,M;Kunkel,SL
通讯作者:
Kunkel,SL
影响因子:
11.2
作者:
Thomassen,MJ;Barna,BP;Rankin,D;Wiedemann,HP;Ahmad,M
通讯作者:
Ahmad,M