00414.2002.—Macrophage-derived cytokines may provoke the in-flammatory response in lung injury. Because macrophage influx is a prominent feature of the cellular inflammatory response accompany-ing the development of bronchopulmonary dysplasia, we hypothe-sized that blocking macrophage influx would reduce overall cellular influx and oxidative damage. Newborn rats were exposed at birth to 95 % O2 or air for 1 wk, 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 histological sections from the 95 % O2-exposed, IgG-injected pups compared with air-exposed controls. At 1 wk, anti-MCP-1-treated pups had reduced leukocy...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72927/1/j.1749-6632.1997.tb46258.x.pd
Valerie Le Rouzic, Kari Wiedinger, Heping ZhouDepartment of Biological Sciences, Seton Hall Universi...
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the ...
Neutrophil influx in lung injury is controlled in part by chemo-kines acting through the receptor, C...
Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well define...
Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well define...
Administration of inhaled nitric oxide (iNO) is a potential therapeutic strategy to prevent bronchop...
AbstractObjectivesActivation of the alveolar macrophage is critical to the development of nonischemi...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72927/1/j.1749-6632.1997.tb46258.x.pd
Valerie Le Rouzic, Kari Wiedinger, Heping ZhouDepartment of Biological Sciences, Seton Hall Universi...
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the ...
Neutrophil influx in lung injury is controlled in part by chemo-kines acting through the receptor, C...
Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well define...
Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well define...
Administration of inhaled nitric oxide (iNO) is a potential therapeutic strategy to prevent bronchop...
AbstractObjectivesActivation of the alveolar macrophage is critical to the development of nonischemi...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
International audienceAcute lung injury and compromised alveolar development characterize bronchopul...
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72927/1/j.1749-6632.1997.tb46258.x.pd