Busam K, Gieringer C, Freudenberg M, Hohmann H P
Institute of Biochemistry, University of Freiburg, Germany.
Infect Immun. 1992 May;60(5):2008-15. doi: 10.1128/iai.60.5.2008-2015.1992.
Heat-killed gram-positive Staphylococcus aureus as well as S. aureus-derived exotoxins B and toxic shock syndrome toxin 1 can induce nuclear factor kappa B (NF-kappa B)-like activity in murine bone marrow macrophages. The induction of NF-kappa B-like activity in murine macrophages by S. aureus was as effective as induction by tumor necrosis factor alpha (TNF-alpha) or lipopolysaccharides (LPS) and was observed in macrophages derived from LPS-sensitive and LPS-resistant mice. Stimulation of macrophages with S. aureus but not with the exotoxins resulted in the accumulation of TNF-alpha in the culture medium. The induction of NF-kappa B-like activity by S. aureus, however, clearly preceded TNF-alpha secretion and was not inhibited by a neutralizing serum against TNF-alpha. In addition, pretreatment of macrophages with the protein synthesis inhibitor cycloheximide or dexamethasone, which prevented the secretion of TNF-alpha from macrophages, did not interfere with the induction of NF-kappa B-like activity by S. aureus. This findings reveal the existence of bacterial components other than LPS which can induce NF-kappa B-like activity in susceptible cells.
热灭活的革兰氏阳性金黄色葡萄球菌以及源自金黄色葡萄球菌的外毒素B和中毒性休克综合征毒素1可在小鼠骨髓巨噬细胞中诱导核因子κB(NF-κB)样活性。金黄色葡萄球菌在小鼠巨噬细胞中诱导的NF-κB样活性与肿瘤坏死因子α(TNF-α)或脂多糖(LPS)诱导的效果一样有效,并且在源自LPS敏感和LPS抗性小鼠的巨噬细胞中均有观察到。用金黄色葡萄球菌而非外毒素刺激巨噬细胞会导致培养基中TNF-α的积累。然而,金黄色葡萄球菌诱导的NF-κB样活性明显先于TNF-α分泌,并且不受抗TNF-α中和血清的抑制。此外,用蛋白质合成抑制剂环己酰亚胺或地塞米松预处理巨噬细胞,可阻止巨噬细胞分泌TNF-α,但这并不干扰金黄色葡萄球菌诱导的NF-κB样活性。这些发现揭示了除LPS之外还存在其他细菌成分,它们可在易感细胞中诱导NF-κB样活性。