Toll样受体介导H37Rv诱导的单核细胞趋化蛋白-1表达

李敏超; 杜先智; 周向东

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Toll样受体介导H37Rv诱导的单核细胞趋化蛋白-1表达

论著 | 更新时间：2026-01-09

- Toll样受体介导H37Rv诱导的单核细胞趋化蛋白-1表达
- Toll-like receptor mediates MCP-1 expression induced by mycobacterium tuberculosis H37Rv
- 陆军军医大学学报 2010年32卷第20期页码：2181-2184
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  中图分类号： R392.32;R394.2;R520.2
- 纸质出版：2010
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李敏超,杜先智,周向东.Toll样受体介导H37Rv诱导的单核细胞趋化蛋白-1表达[J].陆军军医大学学报(原第三军医大学学报),2010,32(20):2181-2184.

　Li Minchao,Du Xianzhi,Zhou Xiangdong.Toll-like receptor mediates MCP-1 expression induced by mycobacterium tuberculosis H37Rv[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(20):2181-2184.
李敏超,杜先智,周向东.Toll样受体介导H37Rv诱导的单核细胞趋化蛋白-1表达[J].陆军军医大学学报(原第三军医大学学报),2010,32(20):2181-2184. DOI：

　Li Minchao,Du Xianzhi,Zhou Xiangdong.Toll-like receptor mediates MCP-1 expression induced by mycobacterium tuberculosis H37Rv[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(20):2181-2184. DOI：

摘要

目的探讨Toll样受体2（TLR2）、TLR4介导的免疫调节信号通路在结核分枝杆菌感染诱导的单核细胞趋化蛋白-1（monocyte chemo attractant protein-1，MCP-1）产生中所起的作用。方法建立人型结核分枝杆菌H37Rv感染小鼠模型，获取模型组及对照组小鼠支气管肺泡灌洗液（bronchoalveolar lavage fluid

BALF）及肺泡巨噬细胞(alveolar macrophage

AM)，对BALF中AM进行计数，采用酶联免疫吸附试验（ELISA）法测定BALF中MCP-1水平，Western免疫蛋白印迹（Western blot）方法检测肺组织中MCP-1蛋白含量，逆转录聚合酶链反应（RT-PCR）测定模型组及对照组AM中TLR2、TLR4 mRNA的表达；抗体干预组的AM用TLR2、TLR4抗体预处理并与H37Rv菌株共培养，并设未予以抗体预处理的PBS组及未作任何处理的对照组，分别用ELISA、Western blot法检测AM培养液中及AM中的MCP-1水平，以观察TLR2、TLR4在H37Rv诱导MCP-1生成所起的作用。结果模型组BALF中AM计数及MCP-1蛋白含量显著高于对照组（P0.05）；模型组小鼠肺组织中MCP-1蛋白含量显著高于对照组（P0.05）；模型组AM内TLR2、TLR4 mRNA表达显著高于对照组（P0.05）；模型组BALF中MCP-1水平与AM数目呈正相关（r=0.92

P0.05），并分别与TLR2、TLR4 mRNA表达呈正相关（r=0.88

P0.05；r=0.82， P0.05）。PBS组AM及其培养上清液中MCP-1蛋白水平显著高于对照组（P0.05）；TLR2、TLR4抗体干预组AM及其培养上清液中MCP-1蛋白水平均显著低于PBS组（P0.05）。结论在结核宿主免疫中，MCP-1参与诱导单核细胞聚集到感染部位这一过程， AM膜上的TLR2、TLR4受体通道介导了人型结核分枝杆菌H37Rv所诱导的MCP-1表达。

Abstract

Objective To explore the role of Toll-like receptor (TLR)2- and TLR4-mediated immune regulating signal pathway on the production of monocyte chemo attractant protein-1 (MCP-1) induced by infection of mycobacterium tuberculosis. Methods Mouse model of H37Rv infection was made by injecting H37Rv through tail vein. Alveolar macrophage (AMs) and bronchoalveolar lavage fluid (BALF) were obtained from H37Rv group and control group. The numbers of AM in BALF were counted. MCP-1 protein levels in BALF and lung tissue were determined by sandwich ELISA and Western blotting respectively. The expression of TLR2 and TLR4 mRNA in AMs were examined by RT-PCR. To investigate the role of TLR2 and TLR4 on the expression of MCP-1 induced by H37Rv

the AMs of antibody intervention group were pretreated with TLR2-antibody/TLR4-antibody and then co-incubated with H37Rv. AMs were pretreated with PBS instead of TLR2-antibody/TLR4-antibody and untreated AMs were regarded as PBS group and control group. MCP-1 protein levels in AM culture supernatants and AM were determined by sandwich ELISA and Western blotting respectively. Results Compared with those of control group

MCP-1 level and AM count in BALF of H37Rv group were increased significantly (P0.05)

and MCP-1 protein level in lung tissue of H37Rv group was increased significantly (P0.05). Expression of TLR2 and TLR4 mRNA in AMs of H37Rv group were higher than those of control group (P0.05). Positive correlation was observed between MCP-1 level and AM count in BALF （r=0.92

P0.05）. Same correlation was found between MCP-1 level in BALF and expressions of TLR2 and TLR4 mRNA in AMs of H37Rv group（r=0.88

P0.05；r=0.82， P0.05）. MCP-1 protein level in AM and AM culture supernatants of PBS group was higher than that of control group and TLR2/ TLR4-antibody intervened group (P0.05). Conclusion MCP-1 is involved in the process of monocytes gathering together to the infection site during host immune to tuberculosis. TLR2/TLR4 receptor channel on AM membrane mediates the expression of MCP-1 induced by H37Rv.

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