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Báo cáo y học: "Inhibition of monocyte chemoattractant protein-1 prevents diaphragmatic inflammation and maintains contractile function during endotoxemi"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Inhibition of monocyte chemoattractant protein-1 prevents diaphragmatic inflammation and maintains contractile function during endotoxemia. | Labbe et al. Critical Care 2010 14 R187 http ccforum.eom content 14 5 R187 c CRITICAL CARE RESEARCH Open Access Inhibition of monocyte chemoattractant protein-1 prevents diaphragmatic inflammation and maintains contractile function during endotoxemia 1 1 1 1.2 1 Katherine Labbe Gawiyou Danialou Dusanka Gvozdic Alexandre Demoule Maziar Divangahi John H Boyd1 3 Basil J Petrof1 3 Abstract Introduction Respiratory muscle weakness is common in sepsis patients. Proinflammatory mediators produced during sepsis have been implicated in diaphragmatic contractile dysfunction but the role of chemokines has not been explored. This study addressed the role of monocyte chemoattractant protein-1 MCP-1 also known as CCL2 in the pathogenesis of diaphragmatic inflammation and weakness during endotoxemia. Methods Mice were treated as follows n 6 per group a saline b endotoxin 25 gg g IP c endotoxin anti-MCP-1 antibody and d endotoxin isotype control antibody. Muscles were also exposed to recombinant MCP-1 in vivo and in vitro. Measurements were made of diaphragmatic force generation leukocyte infiltration and proinflammatory mediator MCP-1 IL-1a IL-1P IL-6 NF-kB expression activity. Results In vivo endotoxin-treated mice showed a large decrease in diaphragmatic force together with upregulation of MCP-1 and other cytokines but without an increase in intramuscular leukocytes. Antibody neutralization of MCP-1 prevented the endotoxin-induced force loss and reduced expression of MCP-1 IL-1a IL-1P and IL-6 in the diaphragm. MCP-1 treatment of nonseptic muscles also led to contractile weakness and MCP-1 stimulated its own transcription independent of NF-kB activation in vitro. Conclusions These results suggest that MCP-1 plays an important role in the pathogenesis of diaphragmatic weakness during sepsis by both direct and indirect mechanisms. We speculate that its immunomodulatory properties and ability to modify skeletal muscle function make MCP-1 a potential therapeutic target in .