Interleukin-8 is a major component of pleural liquid chemotactic activity in a rabbit model of endotoxin pleurisy.
Interleukin-8 is a major component of pleural liquid chemotactic activity in a rabbit model of endotoxin pleurisy.
复制标题
白细胞介素-8 (Interleukin-8) 是兔内毒素性胸膜炎模型中胸膜液趋化活性的主要成分。
DOI：
10.1152/ajplung.1994.267.2.l137
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Broaddus,VC
中科院分区：
文献类型：
--
作者：
Boylan,AM;Hebert,CA;Sadick,M;Wong,WL;Chuntharapai,A;Hoeffel,JM;Hartiala,KT;Broaddus,VC
革兰氏阴性内毒素在体外诱导产生有效的趋化因子白细胞介素-8（IL-8）;然而，IL-8在体内内毒素诱导的炎症中的重要性尚不清楚。我们询问IL-8是否是内毒素引起的急性炎症液体中趋化活性的重要贡献者，以及如果存在，产生的IL-8抗原的浓度。本研究克隆并表达了兔重组IL-8（rrIL-8），制备了特异性抗兔IL-8的单克隆抗体（mAb），并以此为基础建立了检测兔IL-8活性的方法和检测兔IL-8抗原的方法。将大肠杆菌内毒素（20 ng/ml，n = 4，或2，000 ng/ml，n = 4）滴入8只家兔的胸膜腔中6 h。通过在两种不同条件下测量兔嗜中性粒细胞向胸膜液的迁移来测定内毒素胸膜炎样品中的兔IL-8生物活性：1）加入抗IL-8中和mAb后和2）嗜中性粒细胞对rrIL-8脱敏后。加入抗IL-8单克隆抗体使中性粒细胞向胸膜液的迁移减少了65 +/- 13和75 +/- 22%（平均值+/- SE，分别为20和2，000 ng/ml内毒素后;与对照单克隆抗体相比P < 0.01）。中性粒细胞对rrIL-8的脱敏使其向胸膜液的迁移减少了72 +/- 5%（P = 0.03，与中性粒细胞单独暴露于缓冲液相比。（250字处删节）
Gram-negative endotoxin induces production of the potent chemotactic factor interleukin-8 (IL-8) in vitro; however, the importance of IL-8 in endotoxin-induced inflammation in vivo is unknown. We asked whether IL-8 is an important contributor to chemotactic activity in acute inflammatory liquids formed in response to endotoxin, and, if present, what concentrations of IL-8 antigen are generated. For these studies, we cloned and expressed rabbit recombinant IL-8 (rrIL-8), developed specific anti-rabbit IL-8 monoclonal antibodies (mAb), and then used these reagents to develop assays to detect rabbit IL-8 bioactivity and measure rabbit IL-8 antigen. Escherichia coli endotoxin (20 ng/ml, n = 4, or 2,000 ng/ml, n = 4) was instilled into the pleural space of eight rabbits for 6 h. Rabbit IL-8 bioactivity in the endotoxin pleurisy samples was assayed by measuring the migration of rabbit neutrophils toward the pleural liquid under two different conditions: 1) after addition of an anti-IL-8 neutralizing mAb and 2) after desensitization of the neutrophils to rrIL-8. Addition of the anti-IL-8 mAb decreased neutrophil migration toward the pleural liquid by 65 +/- 13 and 75 +/- 22% (mean +/- SE, after 20 and 2,000 ng/ml endotoxin, respectively; P < 0.01 compared with a control mAb). Desensitization of neutrophils to rrIL-8 decreased their migration toward the pleural liquid by 72 +/- 5% (P = 0.03, compared with exposure of neutrophils to buffer alone.(ABSTRACT TRUNCATED AT 250 WORDS)