Inhibition of colony-stimulating factor (CSF) production by postburn serum: negative feedback inhibition mediated by lactoferrin.
Inhibition of colony-stimulating factor (CSF) production by postburn serum: negative feedback inhibition mediated by lactoferrin.
复制标题
烧伤后血清抑制集落刺激因子（CSF）的产生：乳铁蛋白介导的负反馈抑制。
DOI：
10.1097/00005373-198811000-00003
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Bartle,EJ
中科院分区：
文献类型：
--
作者：
Peterson,VM;Ambruso,DR;Emmett,M;Bartle,EJ
集落刺激因子 (CSF) 的产生和粒细胞-巨噬细胞干细胞 (CFU-GM) 的增殖，而严重的脓毒症通常与白细胞减少症相关。造成这些粒细胞生成缺陷的潜在机制尚不清楚，但烧伤后血清已被证明可以抑制脑脊液产生，这一事实表明体液因素或多种因素可能发挥作用。先前的研究表明，乳铁蛋白（LF）（一种已知的脑脊液产生抑制剂）的血浆水平在烧伤后升高。为了确定 LF 是否与血清介导的 CSF 产生抑制有关，使用酶联免疫吸附测定 (ELISA) 连续测量了 18 名烧伤患者的 LF 血浆水平。 LF 在受伤后 24 小时内升高，并与绝对粒细胞增多相关，后者迅速下降，在烧伤后第 3 至 5 天达到最低点。烧伤后血清，尤其是在烧伤后最初 24 小时内收集的血清，可抑制正常人外周血单核细胞在体外产生脑脊液。将烧伤后血清与 LF 抗体预孵育可恢复正常的脑脊液产生。这些数据表明 LF 可能在烧伤后粒细胞生成的调节中发挥重要作用。
in the production of colony-stimulating factor (CSF) and the proliferation of granulocyte-macrophage stem cells (CFU-GM), and overwhelming sepsis is often associated with leukopenia. The underlying mechanisms accounting for these granulopoietic defects are poorly understood, but the fact that postburn serum has been shown to inhibit CSF production suggests that a humoral factor or factors may play a role. Previous work has demonstrated that plasma levels of lactoferrin (LF), a known inhibitor of CSF production, are elevated following burn injury. To determine if LF is responsible for serum-mediated inhibition of CSF production, serial plasma levels of LF were measured in 18 burn patients using an enzyme-linked immunoabsorbent assay (ELISA). LF was elevated within 24 hours of injury and was associated with an absolute granulocytosis which rapidly declined, reaching a nadir at postburn days 3 through 5. Postburn serum, especially when collected during the first 24 hours following burn injury, inhibited in vitro CSF production by normal human peripheral blood mononuclear cells. Pre-incubation of postburn serum with an LF antibody restored normal CSF production. These data suggest that LF may play an important role in the regulation of postburn granulopoiesis.