As expected, mice that were genetically modified so that they did not express CXCR2 (called CXCR2 knockout mice) failed to recruit neutrophils. However, the authors were surprised to find that normal mice whose normal bone marrow cells (ie., immune cells) were replaced with cells from the CXCR2 knockout mice were able to recruit neutrophils to the lung at a rate of about 50% of normal, suggesting that even though the knockout neutrophils did not have CXCR2, they were still able to migrate to the lung. Using a specific antibody that detects CXCR2 protein, the researchers found that CXCR2 is present on blood vessel wall cells of the lung and in cells called epithelial cells that line the airways.
The authors report that it is this pattern of CXCR2 expression on lung cells, and not the presence of CXCR2 on the neutrophils themselves, which is essential for neutrophil recruitment in response to LPS and the resulting acute lung injury.
TITLE: Critical role of endothelial CXCR2 in LPS-induced neutrophil migration into the lung
University of Virginia, Charlottesville, Virginia, USA
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