作者: Joseph A. Kitzmiller , Garry J. Southan , Robert W. Wilmott , Csaba Szabó , Andrew L. Salzman
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摘要: Chronic airway inflammation induced by Pseudomonas aeruginosa is the eventual cause of respiratory failure in most people affected cystic fibrosis. Recent evidence implicates involvement free radical and oxidant stress pathogenesis inflammatory injury. Here we report efficacy a novel experimental therapeutic, mercaptoethylguanidine (MEG), which has combined actions as selective inhibitor inducible nitric oxide synthase scavenger peroxynitrite, potent formed reaction superoxide radical. pulmonary infection was established FVB/N mice intratracheal administration 105 colony-forming units P. agar beads. Treatment with MEG (10 mg/kg/dose every 8 h i.p.) inhibited weight loss first 3 days reduced histologic injury at postinfection. also myeloperoxidase activity, marker neutrophil infiltration, concentrations proinflammatory cytokines interleukin-1β, tumor necrosis factor-α, macrophage protein 2 whole lung homogenates. MEG-treated animals controls had similar perioperative mortality comparable colony counts days, indicating that did not exacerbate infection. Our data suggest may be an effective immunomodulatory therapy chronic