IL-10 Attenuates Inflammation Via MyD88/NF-κB Signal Pathway Depression_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

LAN Yang ^1,2 , LI Li ¹ , YUAN Weifeng ^1,2 , HUANG Wenjie. ¹

Department of Respiratory Medicine, General Hospital of Guangzhou Military Command. Guangzhou, Guangdong, 510010, ChinaCorresponding Author: HUANGWen-jie, E-mail: Huangyelu1029@ VIP.163. com;

Corresponding author：

Keywords：

Interleukin-10; Human myeloid differentiation factor 88; Nuclear factor kappa B

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Objective To investigate the effects of IL-10 on lipopolysaccharide( LPS) -induced MyD88 /NF-κB signaling activation. Methods Ana-1 macrophages were divided into a LPS group and a LPS + IL-10 group. The cells and the culture supernatant were collected at 0, 0. 5, 1, and 2 hours respectively. The expression levels of NF-κB p65 and MyD88 in cytoplasm and nucleus were detected by Western blotting. The concentration of TNF-αin the culture supernatant was determined by ELISA. Results Through 0 to 2 hours, MyD88 expression increased significantly after LPS stimulation. The expression was attenuated by the pretreatment of IL-10, which returned to normal levels at 2 hours( 8. 8 ±0. 3 vs 21. 4 ±1. 8,P lt;0. 05) . IL-10 had no effect on total expression of NF-κB, but decreased nuclei / cytoplasm ratio of NF-κB p65 after LPS stimulation. The ratio was lower in the LPS + IL-10 group compared and the LPS group at 1 hour and 2 hour ( 1. 1 ±0. 1 vs 2. 4 ±0. 4, 0. 6 ±0. 7 vs 3. 1 ±0. 6, P lt; 0. 05) . Consequently, IL-10 pretreatment decreased TNF-α concentration after LPS stimulation at 1 hour and 2 hours [ ( 222. 5 ±33. 5) pg/mL vs ( 365. 2 ±22. 7) pg/mL, ( 212. 7 ±15. 9) pg/mL vs ( 566. 2 ±31. 5) pg/mL, P lt;0. 05] .Conclusion IL-10 attenuates inflammation via MyD88 /NF-κB signal pathway depression.

Citation： LAN Yang,LI Li,YUAN Weifeng,HUANG Wenjie.. IL-10 Attenuates Inflammation Via MyD88/NF-κB Signal Pathway Depression. Chinese Journal of Respiratory and Critical Care Medicine, 2010, 9(3): 243-245. doi: Copy

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1. Inoue G. Effect of interleukin-10 ( IL-10 ) on experimental LPSinduced acute lung injury. J Infect Chemother, 2000 , 6: 51 -60 .
2. 陈业民, 黄文杰, 李胜利, 等. 重症肺炎大鼠干扰素-γ、白细胞介素-6 和肿瘤坏死因子-α含量变化. 中国病理生理杂志, 2007, 23 :492-494.
3. 李胜利, 黄文杰. 地塞米松对SD 大鼠肺炎克雷伯杆菌性重症肺炎模型血清白细胞介素-8、10 的影响. 实用医学杂志, 2007, 23 :2634-2635.
4. Reutershan J, Basit A, Galkina EV, et al. Sequential recruitment of neutrophils into lung and lung injury bronchoalveolar lavage fluid in LPS-induced acute lung injury. Am J Physiol Lung Cell Mol Physiol,2005, 289 : 807-815.
5. Wanidworanun C, Strober W. Predominant role of tumor necrosis factor-alpha in human monocyte IL-10 synthesis. J Immunol, 1993 ,151: 6853 -6861 .
6. Wang P, Wu P, Siegel MI, et al. Interleukin-10 inhibits nuclear factor kappa B( NF kappa B) activation in human monocytes. IL-10 and IL-4 suppress cytokine synthesis by different mechanisms. J Biol Chem,1995, 270 : 9558 -9563 .
7. Schottelius AJ, Mayo MW, Sartor RB, et al. Interleukin-10 signaling blocks inhibitor of kappa B kinase activity and nuclear factor-kappa B DNA binding. J Biol Chem, 1999 , 274: 31868 -31874.
8. Zhang FX, Kirschning CJ, Mancinelli R, et al. Lipopolysaccharide up regulates the expression of Toll-like receptor 4 in human vascular endothelial cells. Chin Med J( Engl) , 2002, 115: 286-289.

Chinese Journal of Respiratory and Critical Care Medicine

IL-10 Attenuates Inflammation Via MyD88/NF-κB Signal Pathway Depression

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