Parsonnet J, Gillis Z A
Channing Laboratory, Brigham and Women's Hospital, Boston, Massachusetts 02115.
J Infect Dis. 1988 Nov;158(5):1026-33. doi: 10.1093/infdis/158.5.1026.
We studied the effect of toxic-shock-syndrome toxin-1 (TSST-1) on production of tumor necrosis factor (TNF) by human monocytes. Adherent mononuclear cells were stimulated with TSST-1 and their supernatants assayed for TNF by using L929 cells in a cytotoxicity assay. TSST-1 stimulated production of TNF over a wide range of concentrations. The cytotoxicity of monocyte supernatants was neutralized by antibody to TNF but not by antibody to interleukin-1 or by normal rabbit serum. TSST-1 and lipopolysaccharide (LPS) had a synergistic effect on monokine production. Monocytes "primed" with TSST-1 produced more interleukin-1 and TNF in response to LPS than did unprimed cells. Treating monocytes with LPS before TSST-1 and co-incubating the two agents with cells for 24 h also enhanced monokine production under some circumstances. These studies suggest a role for TNF in the pathogenesis of toxic shock syndrome, as a consequence of induction by TSST-1 alone or the synergistic effects of several bacterial products.
我们研究了中毒性休克综合征毒素-1(TSST-1)对人单核细胞产生肿瘤坏死因子(TNF)的影响。用TSST-1刺激贴壁单核细胞,并在细胞毒性试验中使用L929细胞检测其培养上清液中的TNF。TSST-1在很宽的浓度范围内均可刺激TNF的产生。单核细胞培养上清液的细胞毒性可被抗TNF抗体中和,但不能被抗白细胞介素-1抗体或正常兔血清中和。TSST-1和脂多糖(LPS)对单核因子的产生具有协同作用。用TSST-1“预处理”的单核细胞对LPS产生的白细胞介素-1和TNF比未预处理的细胞更多。在TSST-1之前先用LPS处理单核细胞,并将这两种试剂与细胞共同孵育24小时,在某些情况下也可增强单核因子的产生。这些研究表明,由于TSST-1单独诱导或几种细菌产物的协同作用,TNF在中毒性休克综合征的发病机制中发挥作用。