PATHOGENESIS OF THE TOXIC SHOCK SYNDROME - T-CELL MEDIATED LETHAL SHOCK CAUSED BY THE SUPERANTIGEN TSST-1

被引:105
作者
MIETHKE, T [1 ]
DUSCHEK, K [1 ]
WAHL, C [1 ]
HEEG, K [1 ]
WAGNER, H [1 ]
机构
[1] TECH UNIV MUNICH, INST MED MICROBIOL & HYG, TROGERSTR 9, W-8000 MUNICH 2, GERMANY
关键词
TOXIC SHOCK SYNDROME; T-CELLS; SUPERANTIGEN;
D O I
10.1002/eji.1830230715
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The pathogenesis of the toxic shock syndrome (TSS) is only incompletely understood. We now present evidence that TSS toxin-I (TSST-1), one of the superantigens produced by Staphylococcus aureus, induces lethal shock in D-galactosamine sensitized mice. In this model TSS is dependent on T cells, since cyclosporin A (CsA) completely blocked development of shock, and since T cell-deficient SCID mice did not show signs of disease upon injection with TSST-1. However, SCID mice repopulated with T cells succumbed to lethal shock. The disease is characterized by a burst of lymphokines like interleukin-2 (IL-2) and tumor necrosis factor (TNF) released into the sera of TSST-1-treated animals. Already 1-2 h after TSST-1 application TNF serum levels peaked and IL-2 levels peaked around 4 h after treatment. TNF appears as key mediator of TSS, because anti-TNF monoclonal antibodies protected TSST-1-challenged mice. Interestingly, the burst of TNF in serum was noted well in advance of detectable markers of T cell activation. Thus, about 5% of all peripheral T cells started to express the IL-2 receptors as late as 4 h after treatment. Comparing TSST-1- and endotoxin-induced shock we conclude that TNF effects shock in both diseases. However, the type of cells involved appears distinct in that T cells cause TSS triggered by the exotosin TSST-1 while macrophages mediate the shock induced by endotoxins.
引用
收藏
页码:1494 / 1500
页数:7
相关论文
共 52 条
[1]   MLS - A RETROVIRUS EXPLOITS THE IMMUNE-SYSTEM [J].
ACHAORBEA, H ;
PALMER, E .
IMMUNOLOGY TODAY, 1991, 12 (10) :356-361
[2]  
BANCROFT GJ, 1989, CURR TOP MICROBIOL, V152, P235
[3]  
BANCROFT GJ, 1989, J IMMUNOL, V143, P127
[4]   PROTECTION OF RABBITS IN AN INFECTION MODEL OF TOXIC SHOCK SYNDROME (TSS) BY A TSS TOXIN-1-SPECIFIC MONOCLONAL-ANTIBODY [J].
BEST, GK ;
SCOTT, DF ;
KLING, JM ;
THOMPSON, MR ;
ADINOLFI, LE ;
BONVENTRE, PF .
INFECTION AND IMMUNITY, 1988, 56 (04) :998-999
[5]   PASSIVE-IMMUNIZATION AGAINST CACHECTIN TUMOR NECROSIS FACTOR PROTECTS MICE FROM LETHAL EFFECT OF ENDOTOXIN [J].
BEUTLER, B ;
MILSARK, IW ;
CERAMI, AC .
SCIENCE, 1985, 229 (4716) :869-871
[6]   STAPHYLOCOCCAL AND STREPTOCOCCAL PYROGENIC TOXINS INVOLVED IN TOXIC SHOCK SYNDROME AND RELATED ILLNESSES [J].
BOHACH, GA ;
FAST, DJ ;
NELSON, RD ;
SCHLIEVERT, PM .
CRITICAL REVIEWS IN MICROBIOLOGY, 1990, 17 (04) :251-272
[7]   NEUTRALIZATION OF TOXIC SHOCK SYNDROME TOXIN-1 BY MONOCLONAL-ANTIBODIES INVITRO AND INVIVO [J].
BONVENTRE, PF ;
THOMPSON, MR ;
ADINOLFI, LE ;
GILLIS, ZA ;
PARSONNET, J .
INFECTION AND IMMUNITY, 1988, 56 (01) :135-141
[8]  
BOSMA M, 1988, CURR TOP MICROBIOL, V137, P197
[9]  
CALLAHAN JE, 1990, J IMMUNOL, V144, P2473
[10]  
CARLSSON R, 1988, J IMMUNOL, V140, P2484