Raponi G, Lun M T, Gaeta A, Ghezzi M C, Nazzari C, Mancini C, Filadoro F, Bartolazzi A, Natali P, Rozenberg-Arska M
I Chair of Clinical Microbiology, Faculty of Medicine, La Sapienza University of Rome, Italy.
J Chemother. 1993 Oct;5(5):317-24. doi: 10.1080/1120009x.1993.11739252.
The capacity of human and murine polyclonal and monoclonal antibodies to inhibit lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) release from human monocytes was investigated. Human pooled immunoglobulin G (IVIG), human IgM monoclonal antibody (HA-1A) directed against the lipid A moiety of LPS, and murine IgG monoclonal antibody (MT-1F) raised in mice against antibiotic-treated Escherichia coli O6:K- were either added simultaneously with LPS to monocytes or preincubated for 1 h at 37 degrees C before being added to monocytes. TNF-alpha content in the monocyte supernatants was then tested. Simultaneous addition of increasing concentrations of IVIG (from 0.3 to 2.5 mg/ml) and 10 micrograms/ml of LPS to monocytes induced an enhanced release of TNF-alpha by monocytes in a dose dependent fashion. Preincubation of IVIG with LPS abolished the additive effect, but did not inhibit LPS-induced TNF-alpha release by monocytes. The simultaneous addition of LPS and HA-1A to monocytes had no additive effect nor did it inhibit TNF-alpha release. On the other hand, inhibition of TNF-alpha release was observed when HA-1A was preincubated with LPS before being added to monocytes. In all instances MT-1F inhibited TNF-alpha release when the monocytes were stimulated with smooth type LPS, but not with LPS isolated from rough mutants.
研究了人源和鼠源多克隆及单克隆抗体抑制脂多糖(LPS)诱导人单核细胞释放肿瘤坏死因子-α(TNF-α)的能力。人混合免疫球蛋白G(IVIG)、针对LPS脂质A部分的人IgM单克隆抗体(HA-1A)以及在小鼠体内针对经抗生素处理的大肠杆菌O6:K-产生的鼠IgG单克隆抗体(MT-1F),要么与LPS同时添加到单核细胞中,要么在37℃预孵育1小时后再添加到单核细胞中。然后检测单核细胞上清液中的TNF-α含量。向单核细胞中同时添加浓度递增的IVIG(从0.3至2.5mg/ml)和10μg/ml LPS,可诱导单核细胞以剂量依赖方式增强TNF-α的释放。IVIG与LPS预孵育消除了相加效应,但未抑制LPS诱导的单核细胞TNF-α释放。向单核细胞中同时添加LPS和HA-1A既无相加效应,也不抑制TNF-α释放。另一方面,当HA-1A在添加到单核细胞之前与LPS预孵育时,观察到TNF-α释放受到抑制。在所有情况下,当单核细胞用光滑型LPS刺激时,MT-1F抑制TNF-α释放,但用从粗糙突变体分离的LPS刺激时则不然。