对β趋化因子受体CCR1进行靶向破坏可预防胰腺炎相关的肺损伤。
Targeted disruption of the beta-chemokine receptor CCR1 protects against pancreatitis-associated lung injury.
作者信息
Gerard C, Frossard J L, Bhatia M, Saluja A, Gerard N P, Lu B, Steer M
机构信息
Ina Sue Perlmutter Laboratory, Children's Hospital, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School and the Center for Blood Research, Boston, Massachusetts 02115, USA.
出版信息
J Clin Invest. 1997 Oct 15;100(8):2022-7. doi: 10.1172/JCI119734.
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 MIP1alpha and RANTES. Genetic deletion of one of the MIP1alpha and RANTES receptors, CCR5, is associated with protection from infection with HIV-1 in humans, while deletion of the ligand MIP1alpha protects against Coxsackie virus-associated myocarditis. In this report we show that the deletion of another receptor for MIP1alpha 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.
β-趋化因子及其受体介导包括淋巴细胞和巨噬细胞在内的多种白细胞的运输和激活。已鉴定出不少于八种β-趋化因子受体，其中四种能够识别趋化因子MIP1α和RANTES。MIP1α和RANTES受体之一CCR5的基因缺失与人类对HIV-1感染的抵抗力相关，而配体MIP1α的缺失可预防柯萨奇病毒相关性心肌炎。在本报告中，我们表明，另一种MIP1α和RANTES受体CCR1受体的缺失与小鼠急性胰腺炎继发的肺部炎症的预防相关。对肺损伤的保护作用与TNF-α水平的降低呈时间顺序相关，表明CCR1受体的激活是全身炎症反应综合征中的早期事件。
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