Monodane T, Kawabata Y, Yang S, Hase S, Takada H
Department of Microbiology and Immunology, Kagoshima University Dental School, Kagoshima 890-8544, *Department of Microbiology and Immunology, Tohoku University School of Dentistry, Sendai 980-8575 and †Department of Chemistry, Graduate School of Science, Osaka University, Toyonka 560-0043, Japan.
J Med Microbiol. 2001 Jan;50(1):4-12. doi: 10.1099/0022-1317-50-1-4.
Earlier studies showed that Micrococcus luteus cells and cell walls induced anaphylactoid reactions leading to death, in some instances within 1 h, in C3H/HeN mice primed with muramyl dipeptide (MDP). They also induced serum cytokines in the surviving mice. The present study investigated the structural components responsible for these activities. Teichuronic acids, a component of M. luteus cell walls, induced tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in MDP-primed C3H/HeN mice. Peptidoglycans had little effect on the cytokine-inducing activities. Reducing teichuronic acids, i.e., teichuronic acids whose carboxyl groups had been reduced, lost their cytokine-inducing activities. Neither peptidoglycans nor teichuronic acids induced anaphylactoid reactions in the MDP-primed mice. Purified teichuronic acids also induced TNF-alpha and IL-6 production in C3H/HeN murine peritoneal macrophages and human whole-blood cells in the culture, but reduced teichuronic acids did not. The purified teichuronic acids induced no TNF-alpha and only low levels of IL-6 in MDP-primed C3H/HeJ mice, and neither cytokine in peritoneal macrophage cultures from C3H/HeJ mice with a single point of mutation in Toll-like receptor 4 (TLR4) gene. These findings suggest that induction of cytokines by teichuronic acids is mainly TLR4-dependent.
早期研究表明,在经胞壁酰二肽(MDP)致敏的C3H/HeN小鼠中,藤黄微球菌细胞和细胞壁可引发类过敏反应,导致死亡,在某些情况下1小时内即会发生。它们还会在存活小鼠体内诱导血清细胞因子产生。本研究调查了负责这些活性的结构成分。磷壁醛酸是藤黄微球菌细胞壁的一种成分,可在经MDP致敏的C3H/HeN小鼠中诱导肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)产生。肽聚糖对细胞因子诱导活性影响很小。还原型磷壁醛酸,即羧基已被还原的磷壁醛酸,失去了其细胞因子诱导活性。肽聚糖和磷壁醛酸在经MDP致敏的小鼠中均未引发类过敏反应。纯化的磷壁醛酸还可在培养中的C3H/HeN小鼠腹膜巨噬细胞和人全血细胞中诱导TNF-α和IL-6产生,但还原型磷壁醛酸则不能。纯化的磷壁醛酸在经MDP致敏的C3H/HeJ小鼠中未诱导TNF-α产生,仅诱导了低水平的IL-6,在Toll样受体4(TLR4)基因有单点突变的C3H/HeJ小鼠的腹膜巨噬细胞培养物中均未诱导这两种细胞因子产生。这些发现表明,磷壁醛酸诱导细胞因子主要依赖TLR4。