Targeted disruption of the beta-chemokine receptor CCR1 protects against pancreatitis-associated lung injury

被引:174
作者
Gerard, C
Frossard, JL
Bhatia, M
Saluja, A
Gerard, NP
Lu, B
Steer, M
机构
[1] HARVARD UNIV,CHILDRENS HOSP,SCH MED,BETH ISRAEL DEACONNESS MED CTR,DEPT PEDIAT,BOSTON,MA 02115
[2] BETH ISRAEL DEACONNESS MED CTR,DEPT SURG,BOSTON,MA 02215
[3] HARVARD UNIV,SCH MED,BOSTON,MA 02215
关键词
MIP1 alpha/RANTES receptor; caerulein; gene deletion; respiratory distress; systemic immune response syndrome;
D O I
10.1172/JCI119734
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
beta-Chemokines and their receptors mediate the trafficking and activation of a variety of leukocytes including the lymphocyte and macrophage. An array of no less than eight beta-chemokine receptors has been identified, four of which are capable of recognizing the chemokines MIP1 alpha and RANTES. Genetic deletion of one of the MIP1 alpha and RANTES receptors, CCR5, is associated with protection from infection with HIV-1 in humans, while deletion of the ligand MIP1 alpha protects against Coxsackie virus-associated myocarditis. In this report we show that the deletion of another receptor for MIP1 alpha and RANTES, the CCR1 receptor, is associated with protection from pulmonary inflammation secondary to acute pancreatitis in the mouse. The protection from lung injury is associated with decreased levels of TNF-alpha in a temporal sequence indicating that the activation of the CCR1 receptor is an early event in the systemic inflammatory response syndrome.
引用
收藏
页码:2022 / 2027
页数:6
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