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白细胞介素-6(IL-6)而非肿瘤坏死因子-α(TNF-α)可增加人体血浆 YKL-40 水平。

IL-6, but not TNF-α, increases plasma YKL-40 in human subjects.

机构信息

The Centre of Inflammation and Metabolism, Department of Infectious Diseases and CMRC, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, Denmark.

出版信息

Cytokine. 2011 Jul;55(1):152-5. doi: 10.1016/j.cyto.2011.03.014. Epub 2011 Apr 7.

DOI:10.1016/j.cyto.2011.03.014
PMID:21478032
Abstract

Plasma levels of YKL-40 are elevated in patients with systemic infection, inflammatory disorders and cancer. Both monocytes/macrophages, neutrophils, and cancer cells have the capacity to produce YKL-40, but the regulation during the inflammatory response is unknown. To study the possible role of interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α in the regulation of YKL-40 plasma levels, we included healthy men, who received either recombinant human (rh)IL-6 (n=6), rhTNF-α (n=8) or vehicle (n=7) for 3h. The plasma levels of IL-6 and TNF-α reached ∼ 150 and ∼ 18 pg/ml, respectively, during the infusions. Following the IL-6 infusion, the plasma level of YKL-40 increased from ∼ 30 to ∼ 57 ng/ml (p<0.05) at 24h, and returned to normal values after 48 h. The plasma level of YKL-40 did not change during TNF-α infusion or infusion of vehicle. These data demonstrate that IL-6, but not TNF-α, has a key-role in the regulation of plasma YKL-40 levels during inflammation.

摘要

YKL-40 蛋白在患有全身感染、炎症性疾病和癌症的患者中的血浆水平升高。单核细胞/巨噬细胞、中性粒细胞和癌细胞均具有产生 YKL-40 的能力,但在炎症反应期间的调控机制尚不清楚。为了研究白细胞介素 6 (IL-6) 和肿瘤坏死因子 (TNF)-α 可能在 YKL-40 血浆水平调控中的作用,我们纳入了健康男性,他们分别接受重组人 (rh)IL-6(n=6)、rhTNF-α(n=8)或载体(n=7)输注 3 小时。在输注过程中,IL-6 和 TNF-α 的血浆水平分别达到约 150 和 18 pg/ml。在 IL-6 输注后,YKL-40 的血浆水平在 24 小时内从约 30 增加到约 57 ng/ml(p<0.05),并在 48 小时后恢复正常。在 TNF-α 输注或载体输注期间,YKL-40 的血浆水平没有变化。这些数据表明,IL-6 而不是 TNF-α,在炎症期间调节 YKL-40 血浆水平中起关键作用。

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