中毒性休克综合征毒素-1加速小鼠胶原诱导性关节炎。

Toxic shock syndrome toxin-1 accelerated collagen-induced arthritis in mice.

作者信息

Kageyama Y, Koide Y, Nagata T, Uchijima M, Yoshida A, Arai T, Miura T, Miyamoto C, Nagano A

机构信息

Department of Orthopedic Surgery, Hamamatsu University School of Medicine, Hamamatsu, Japan.

出版信息

J Autoimmun. 2001 Mar;16(2):125-31. doi: 10.1006/jaut.2000.0470.

DOI:10.1006/jaut.2000.0470

PMID:11247638

Abstract

The aim of this study was to explore the roles of toxic shock syndrome toxin-1 (TSST-1) in collagen-induced arthritis (CIA). DBA/1 mice were immunized with type II collagen (CII) and treated with TSST-1. Intraperitoneal and intravenous injections of TSST-1 aggravated CIA, enhancing its incidence and severity. CIA was accompanied by an increase in anti-CII IgG Ab levels. Intraperitoneal administration with TSST-1 enhanced IFN-gamma, TNF-alpha, and IL-4 production in DBA/1 mice. We discovered the mRNA expressions of IFN-gamma, IL-2, TNF-alpha, IL-1beta, and iNOS in spleen cells stimulated with TSST-1 in vitro. However, IL-12 and IL-4 mRNA expression were seen constitutively without stimulation. Only a little increase of IL-12 and IL-4 mRNA expression was seen at 2-3 h after treatment with TSST-1. Our experiments demonstrated that CIA was aggravated by the treatment with TSST-1, which may have induced various proinflammatory cytokines and the production of both Th1 and Th2 cytokines.

摘要

本研究的目的是探讨中毒性休克综合征毒素-1（TSST-1）在胶原诱导性关节炎（CIA）中的作用。用II型胶原（CII）免疫DBA/1小鼠并用TSST-1进行处理。腹腔内和静脉内注射TSST-1会加重CIA，提高其发病率和严重程度。CIA伴有抗CII IgG抗体水平升高。腹腔内给予TSST-1可增强DBA/1小鼠中IFN-γ、TNF-α和IL-4的产生。我们发现体外经TSST-1刺激的脾细胞中IFN-γ、IL-2、TNF-α、IL-1β和iNOS的mRNA表达。然而，IL-12和IL-4 mRNA表达在未受刺激时即有组成性表达。在用TSST-1处理后2至3小时，仅观察到IL-12和IL-4 mRNA表达有少量增加。我们的实验表明，TSST-1处理会加重CIA，这可能诱导了多种促炎细胞因子以及Th1和Th2细胞因子的产生。