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1 Department of Pediatrics, Duke University Medical Center, Durham, NC, USA
2 Department of Pediatrics, Duke University Medical Center, Durham, NC, USA; Comprehensive Center for Inflammatory Disorders, University of North Carolina School of Medicine, Chapel Hill, NC, USA
* To whom correspondence should be addressed. E-mail: auten{at}duke.edu.
Macrophage-derived cytokines may provoke the inflammatory response in lung injury. Because macrophage influx is a prominent feature of the cellular inflammatory response accompanying the development of bronchopulmonary dysplasia, we hypothesized that blocking macrophage influx would reduce overall cellular influx and oxidative damage. Newborn rats were exposed at birth to 95%O2 or air for one week, and hyperoxia-exposed pups were injected with anti-monocyte chemoattractant protein-1 (MCP-1) or IgG control on days 3-5. MCP-1 was increased in bronchoalveolar lavage fluid and in histologic sections from the 95%O2-exposed, IgG-injected pups compared with air-exposed controls. At one week, anti-MCP-1 treated pups had reduced leukocyte numbers, both macrophages and neutrophils, in bronchoalveolar lavage fluid compared with IgG-treated controls. Cytokine-induced neutrophil chemoattractant-1, the rat analog of IL-8, was not significantly decreased in lavage fluid but was decreased in lung cells in anti-MCP-1 treated pups. Tissue carbonyls, a measure of protein oxidation, were decreased in anti-MCP-1 treated pups. Anti-MCP-1 treatment prevented neutrophil influx and reduced protein oxidation in hyperoxia-exposed newborn rats.
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