CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS

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CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS

中国医学科学杂志（英文版） 2006年0卷第3期页码：152-156

Updated：2024-04-10

- CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS
- Affiliations：
- Author bio：
- Funds：
  
  Supported by the National Natural Sciences Foundation of China(30470767,30470768)
- DOI：
  中图分类号： R563
- 纸质出版日期：2006
- Accepted：
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CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS[J]. 中国医学科学杂志（英文版）, 2006,0(3):152-156.

CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS[J]. Chinese medical sciences journal, 2006, 0(3): 152-156.
CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS[J]. 中国医学科学杂志（英文版）, 2006,0(3):152-156. DOI：

CXC CHEMOKINE RECEPTOR 3 MODULATES BLEOMYCIN-INDUCED PULMONARY INJURY VIA INVOLVING INFLAMMATORY PROCESS[J]. Chinese medical sciences journal, 2006, 0(3): 152-156. DOI：

摘要

Abstract

Objective To investigate the role of CXC chemokine receptor 3 （CXCR3） in bleomycin-induced lung injury by using CXCR3 gene deficient mice. Methods Sex-

age-

and weight-matched C57BL/6 CXCR3 gene knockout mice and C57BL/6 wide type mice were challenged by injection of bleomycin via trachea. Lung tissue was stained with HE method. Airway resistance was measured. Bronchoalveolar lavage （BAL） was performed using phosphate buffered saline twice

cell number and differentials were counted by Diff-Quick staining. Interleukin（IL）-4

IL-5

IL-12p40

and interfon-γ in BAL fluid and lung homogenate were measured by enzyme-linked immunosorbent assay. Unpaired t test was explored to compare the difference between two groups. Results On day 7 after bleomycin injection via trachea

CXCR3 knockout mice were protected from bleomycin-induced lung injury as evidenced by fewer accumulation of inflammatory cells in the airway and lung interstitium compared with their wild type littermates （P<0.05）. Airway resistance was also lower in CXCR3 knockout mice compared with wild type mice （P<0.01）. Significantly lower level of inflammatory cytokines release

including the altered production of IL-4 and IL-5 both in BAL fluid and lung tissue was seen in CXCR3 knockout mice than in wild type mice （both P<0.05）.Conclusion CXCR3 signaling promotes inflammatory cells recruiting and initiates inflammatory cytokines cascade following endotracheal bleomycin administration

indicating that CXCR3 might be a therapeutic target for pulmonary injury.

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