Marked reduction of LL-37/hCAP-18, an antimicrobial peptide, in patients with acute myeloid leukemia
Marked reduction of LL-37/hCAP-18, an antimicrobial peptide, in patients with acute myeloid leukemia
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DOI：
10.1532/ijh97.a10407
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发表时间：
2005-01-01
影响因子：
2.1
通讯作者：
Wu, KF
中科院分区：
文献类型：
--
作者：
An, LL;Ma, XT;Wu, KF
我们检测了50例健康献血员和143例各种血液病患者外周血涂片中LL-37/hCAP-18的表达。与健康供者比较。在急性髓系白血病（AML）患者中，尤其是感染患者中，中性粒细胞中的蛋白表达显著降低。而mRNA水平无显著性差异。我们在用脂多糖或金黄色葡萄球菌科万菌株处理的U937细胞中没有检测到LL-37/hCAP-18蛋白表达的增加。此外，LL-37/hCAP-18蛋白的生产没有恢复在分化的髓系细胞系NB 4或HL-60诱导的全反式维甲酸。LL-37/hCAP-18已被证明在宿主防御中发挥作用。AML患者中该基因的缺失可能是AML患者易感染的原因之一。这些病人。(C)2005日本血液学会。
We detected LL-37/hCAP-18 expression in the peripheral blood smears of 50 healthy donors and 143 patients with various hematological diseases. Compared with that in the healthy donors. expression of the protein in the neutrophils was significantly lower in patients with acute myeloid leukemia (AML), especially those with infection. but no significant difference was detected in messenger RNA level. We did not detect increased LL-37/hCAP-18 protein expression in U937 cells treated with lipopolysaccharide or Staphylococcus aureus Cowan strain. Furthermore, LL-37/hCAP-18 protein production was not restored in differentiated myeloid cell lines NB4 or HL-60 induced by all-trans retinoic acid. LL-37/hCAP-18 has been;shown to play, a role in host defense. and its deficiency in AML may be one of the explanations for susceptibility to infection among. these patients. (C) 2005 The Japanese Society of Hematology.