Interleukin-10 reduces the endotoxin-induced hyperalgesia in mice

被引：54

作者：

Kanaan, SA

Poole, S

Saadé, NE

Jabbur, S

Safieh-Garabedian, B

机构：

[1] Amer Univ Beirut, Fac Arts & Sci, Dept Biol, Beirut, Lebanon

[2] Natl Inst Biol Stand & Controls, Div Endocrinol, Potters Bar EN6 3QG, Herts, England

[3] Amer Univ Beirut, Fac Med, Dept Physiol, Beirut, Lebanon

[4] Amer Univ Beirut, Fac Med, Dept Human Morphol, Beirut, Lebanon

来源：

JOURNAL OF NEUROIMMUNOLOGY | 1998年 / 86卷 / 02期

关键词：

IL-10; IL-1; beta; TNF alpha; NGF; hyperalgesia; inflammation;

D O I：

10.1016/S0165-5728(98)00027-7

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

In the endotoxin-induced inflammation, interleukin-10 reduced significantly, and in a dose-dependent manner, the inflammatory pain as assessed by mechanical and thermal tests. The levels of Tumour Necrosis Factor (TNF)alpha and NGF were upregulated at 1.5 h whereas those of IL-1 beta at 6 h after ET injection. IL-10 downregulated the levels of TNF alpha (from 4974.75 +/- 875.78 to 1008 +/- 350 pg/hind paw), NGF (from 352.9 +/- 46.7 to 33.9 +/- 2.4 pg/hind paw) and IL-1 beta (from 2773.88 +/- 423.96 to 1108 +/- 399.56 pg/hind paw). These data suggest that IL-10 inhibits ET-induced hyperalgesia by downregulation of TNF alpha, IL-1 beta and NGF production. (C) 1998 Elsevier Science B.V. All rights reserved.

引用

页码：142 / 150

页数：9

共 49 条

[11]

Fantuzzi G, 1996, J IMMUNOL, V157, P291

[12] BRADYKININ INITIATES CYTOKINE-MEDIATED INFLAMMATORY HYPERALGESIA [J].