烧伤合并内毒素血症骨髓粒单系造血变化及其机制的探讨

目的：探讨烧伤合并内毒素血症骨髓粒单系造血变化及其机制。方法：采用细胞计数和细胞培养观测20％总体表面积Ⅲ度烧伤合并内毒素（按体重1μg/g）腹腔注射后（烧注组）1周内小鼠外周血粒细胞和单核细胞总数及骨髓粒－巨噬细胞集落形成单位（CFU－GM）的动脉变化；同时用免疫组织化学和放射免疫法检测骨髓细胞环氧化酶－2（COX－2）和转化生长因子－β1（TGF－β1）表达及骨髓细胞上清前列腺素E2（PEG2）含量变化。结果：烧注后6小时内外周血粒细胞和单核细胞总数、骨髓CFU－GM略增多，以后逐渐减少，外周血粒细胞和单核细胞总数在1－5日、骨髓CFU－GM在12小时－5日显著低于正常对照组。烧注后1、3日骨髓细胞COX－2和TGF－β1表达明显增强，12小时－5日PGE2显著高于正常对照组，PGE2与CFU－GM呈显著负相关。结论：烧伤合并内毒素血症骨髓粒单系造血抑制；PGE2可能在烧伤合并内毒素血症骨髓粒单系抑制中起重要作用；TGF－β1可能也是粒单系抑制的原因之一。

Changes and mechanism of bone marrow granulopoiesis after burns combined with endotoxemia in mice

Objective:To investigate changes and mechanism of bone marrow granulopoiesis after burns combined with endotoxemia in mice.Methods:Circulating granulocytes and monocytes were counted and colony forming unit-granulocyte/macrophage(CFU-GM) culture was performed in mice sustained 20% total body surface area(TBSA) full-thickness burn injury combined with endotoxin (LPS,1　μg/g body weight) injection during a period of 7 days.Meanwhile,the expressions of cyclooxygenase(COX-2) and transforming growth factor-β1(TGF-β1) of blood mono-nuclear cell(BMNC) were determined with immunohistochemistry,and levels of prostaglandin E2（PGE2) in BMNC supernatant were determined with radioimmunoassay.Results:Circulating granulocytes,monocytes and bone marrow CFU-GM increased slightly within 6 hours after burn injury combined with LPS injection,then decreased gradually.Circulating granulocytes and monocytes were significantly lower from day 1 to day 5,and bone marrow CFU-GM were significantly lower from 12th hour to day 5 when compared with those in control.The expression of COX-2 and TGF-β1 in BMNC were increased from day 1 to day 3 after burns combined with LPS injection.PGE2 levels in BMNC supernatant increased from 12th hour to day 5.Moreover,negative correlation was found between PGE2 and CFU-GM.Conclusions:Bone marrow granulopoiesis was suppressed after burns combined with endotoxemia,and PGE2 might play a pivotal role in the pathophysiological process.TGF-β1 might be one of the contributing factors in granulopoiesis suppression.