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首頁> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Involvement of Kupffer cells in lipopolysaccharide-induced rapid accumulation of platelets in the liver and the ensuing anaphylaxis-like shock in mice
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Involvement of Kupffer cells in lipopolysaccharide-induced rapid accumulation of platelets in the liver and the ensuing anaphylaxis-like shock in mice

機譯：庫普弗細胞參與脂多糖誘導的肝中血小板的快速積累和隨之產生的過敏反應樣休克

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Intravenous injection of Klebsiella 03 lipopolysaccharide (LPS) into BALM mice induces an anaphylaxis-like shock within minutes. Using 5-hydroxytryptamine as a marker for platelets, we previously suggested that a rapid platelet accumulation in the liver and lung precedes the shock, and that a complement-dependent platelet-degradation is involved in the shock. Here, we examined (i) the effect of platelet-depletion (using an anti-platelet monoclonal antibody) on the shock and (ii) the contribution of macrophages to the platelet-accumulation in those organs. LPS-induced platelet-accumulations in the liver and lung were confirmed by immunostaining. In platelet-depleted mice, the shock was largely prevented. The number of F4/80-positive macrophages was much greater in liver than in lung, and the hepatic macrophages were largely lost in mice given clodronate-encapsulated liposomes. In mice treated with such liposomes, both the LPS-induced accumulation of platelets in the liver (but not in the lung) and the shock were largely prevented, and repopulation of hepatic macrophages restored these LPS-induced responses. These results suggest that (i) platelets are indeed involved in the shock, (ii) Kupffer cells mediate the hepatic platelet accumulation, and (iii) preventing this hepatic accumulation can largely prevent rapid shock being induced by LPS (at the dose used here). (c) 2005 Elsevier B.V. All rights reserved.
機譯：向BALM小鼠靜脈內注射Klebsiella 03脂多糖（LPS）會在幾分鐘內引起類似過敏反應的休克。使用5-羥色胺作為血小板的標志物，我們以前曾建議在休克之前先在肝臟和肺中快速積聚血小板，休克涉及血小板依賴的血小板降解。在這里，我們檢查了（i）血小板減少（使用抗血小板單克隆抗體）對休克的影響，以及（ii）巨噬細胞對那些器官中血小板聚集的作用。通過免疫染色證實了LPS誘導的肝和肺中血小板積累。在貧血小板的小鼠中，很大程度上避免了休克。肝中F4 / 80陽性巨噬細胞的數量遠多于肺，給予氯膦酸鹽包封脂質體的小鼠肝巨噬細胞大量丟失。在用此類脂質體治療的小鼠中，LPS誘導的血小板在肝臟（而非肺部）的蓄積和休克都得到了很大的阻止，并且肝巨噬細胞的重新聚集恢復了這些LPS誘導的反應。這些結果表明，（i）血小板確實參與了休克，（ii）庫普弗細胞介導肝血小板積聚，（iii）防止這種肝積聚可以很大程度上防止LPS引起的快速休克（按此處使用的劑量） 。 （c）2005 Elsevier B.V.保留所有權利。

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