白细胞介素-1β和肿瘤坏死因子-α会增加豚鼠气管的微血管渗漏。

Interleukin-1beta and tumour necrosis factor-alpha increase microvascular leakage in the guinea pig trachea.

作者信息

Reynolds Ann M, Holmes Mark D, Scicchitano Raffaele

机构信息

Lung Research Laboratory, Royal Adelaide Hospital, Adelaide, South Australia, Australia.

出版信息

Respirology. 2002 Mar;7(1):23-8. doi: 10.1046/j.1440-1843.2002.00362.x.

DOI:10.1046/j.1440-1843.2002.00362.x

PMID:11896897

Abstract

OBJECTIVE

Airway microvascular leakage is considered to be an important component of airway inflammation in asthma. In the present study we examined the effect of interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNFalpha) on airway microvascular leakage in vivo.

METHODOLOGY

Tracheal Evans blue extravasation was examined in an isolated tracheal segment, in anaesthetized mechanically ventilated guinea pigs. Baseline tracheal microvascular leakage was measured in five animals. As a control group for aerosol challenge, the isolated tracheal segment (n = 5) underwent saline aerosol challenge. To test whether a combination of IL-1beta (10 ng/mL) and TNFalpha (100 ng/mL) induced Evans blue extravasation, the trachea was exposed to an aerosol of these cytokines (n = 5). As a positive control the tracheal segment was challenged with histamine aerosol (5 x 10(-2) mol) (n = 3). All aerosol challenges were for 1 min.

RESULTS

TNFalpha and IL-1beta aerosol challenge significantly increased Evans blue extravasation (28.9 +/- 1.6 microg/g wet tissue, mean +/- SE) compared to saline challenge (13.8 +/- 3.0 microg/g; P < 0.05). Tracheal dye extravasation without aerosol challenge, was not significantly different from saline-challenged animals (17.5 +/- 2.9 and 13.8 +/- 3.0 microg/g, respectively). Histamine significantly increased Evans blue extravasation (50.1 +/- 4.8 microg/g; P < 0.05) compared to saline challenge.

CONCLUSION

Pro-inflammatory cytokines, TNFalpha and IL-1beta are able to induce significant microvascular leakage in the guinea pig trachea.

摘要

目的

气道微血管渗漏被认为是哮喘气道炎症的一个重要组成部分。在本研究中，我们检测了白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNFα）对体内气道微血管渗漏的影响。

方法

在麻醉状态下机械通气的豚鼠中，对分离的气管段进行伊文思蓝渗出检测。测量了5只动物的基线气管微血管渗漏情况。作为气雾剂激发的对照组，对分离的气管段（n = 5）进行盐水气雾剂激发。为了测试IL-1β（10 ng/mL）和TNFα（100 ng/mL）联合使用是否会诱导伊文思蓝渗出，将气管暴露于这些细胞因子的气雾剂中（n = 5）。作为阳性对照，用组胺气雾剂（5×10⁻² mol）对气管段进行激发（n = 3）。所有气雾剂激发均持续1分钟。

结果

与盐水激发相比，TNFα和IL-1β气雾剂激发显著增加了伊文思蓝渗出（28.9±1.6 μg/g湿组织，均值±标准误）（盐水激发为13.8±3.0 μg/g；P < 0.05）。未进行气雾剂激发时的气管染料渗出与盐水激发组动物无显著差异（分别为17.5±2.9和13.8±3.0 μg/g）。与盐水激发相比，组胺显著增加了伊文思蓝渗出（50.1±4.8 μg/g；P < 0.05）。