Rovai L E, Herschman H R, Smith J B
Department of Pediatrics, University of California at Los Angeles School of Medicine 90095-1752, USA.
J Leukoc Biol. 1998 Oct;64(4):494-502. doi: 10.1002/jlb.64.4.494.
Lipopolysaccharide-induced CXC chemokine (LIX) is a novel murine neutrophil-chemoattractant CXC chemokine cloned as a glucocorticoid-attenuated response gene. We investigated LIX message expression in an acute endotoxemia model. LIX message peaks later than KC or macrophage inflammatory protein-2 (MIP-2) and remains elevated longer in almost all tissues. Induced LIX message expression in heart is 5- to 6-fold greater than in lung and spleen, and 20-fold greater than in liver. In contrast, KC expression is equal in heart, lung, and liver, whereas MIP-2 expression is strongest in the lung. Glucocorticoid regulation of these genes also differs. Endotoxemia-induced LIX message expression in the lung is markedly enhanced in adrenalectomized mice and strongly attenuated by dexamethasone, whereas lung KC and MIP-2 expression are unaffected by glucocorticoids. It is surprising to note that endotoxemia-induced brain expression of LIX (but not KC or MIP-2) is increased by dexamethasone. These observations suggest that LIX may have biological roles distinct from KC and MIP-2.
脂多糖诱导的CXC趋化因子（LIX）是一种新的小鼠嗜中性粒细胞趋化性CXC趋化因子，作为一种糖皮质激素减弱反应基因被克隆出来。我们在急性内毒素血症模型中研究了LIX信息表达。LIX信息的峰值出现时间比KC或巨噬细胞炎性蛋白-2（MIP-2）晚，并且在几乎所有组织中保持升高的时间更长。心脏中诱导的LIX信息表达比肺和脾脏中的高5至6倍，比肝脏中的高20倍。相比之下，KC在心脏、肺和肝脏中的表达相同，而MIP-2在肺中的表达最强。糖皮质激素对这些基因的调节也有所不同。在内毒素血症诱导的肺中，LIX信息表达在肾上腺切除的小鼠中显著增强，并被地塞米松强烈减弱，而肺中KC和MIP-2的表达不受糖皮质激素影响。值得注意的是，地塞米松会增加内毒素血症诱导的大脑中LIX（而非KC或MIP-2）的表达。这些观察结果表明，LIX可能具有与KC和MIP-2不同的生物学作用。
