期刊
INFECTION AND IMMUNITY
卷 68, 期 7, 页码 4289-4296出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.68.7.4289-4296.2000
关键词
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资金
- NHLBI NIH HHS [HL57243, K08 HL004421, HL58200, R01 HL057243, R37 HL035276, K08 HL004220, HL50057] Funding Source: Medline
Pulmonary infection due to Pseudomonas aeruginosa has emerged as a leading cause of mortality. A vigorous host response is required to effectively clear the organisms from the lungs. This host defense is dependent on the recruitment and activation of neutrophils and macrophages, A family of chemotactic cytokines (chemokines) has been shown to participate in this protective response. In this study, we assessed the role of the ELR+ (glutamic acid-leucine arginine motif positive) CXC chemokines and their CXC chemokine receptor (CXCR2) in lung antibacterial host defense. The intratracheal administration of Pseudomonas to mice resulted in the time-dependent influx of neutrophils to the lung, peaking at 12 to 24 h after inoculation. The influx of neutrophils was associated with a similar time-dependent expression of the ELR+ CXC chemokines, KC, macrophage inflammatory protein 2 (MIP-2), and lipopolysaccharide-induced CXC chemokine (LIX). Selective neutralization of MIP-2 or KC resulted in modest changes in neutrophil influx but no change in bacterial clearance or survival. However, neutralization of CXCR2 resulted in a striking increase in mortality, which was associated with a marked decrease in neutrophil recruitment and bacterial clearance. Conversely, the site-specific transgenic expression of KC resulted in enhanced clearance of bacteria after Pseudomonas challenge. This study indicates that ELR+ CXC chemokines are critical mediators of neutrophil-mediated host defense in Pseudomonas pneumonia.
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