Ferrante A, Staugas R E, Rowan-Kelly B, Bresatz S, Kumaratilake L M, Rzepczyk C M, Adolf G R
Department of Immunology, University of Adelaide Department of Paediatrics, South Australia.
Infect Immun. 1990 Dec;58(12):3996-4003. doi: 10.1128/iai.58.12.3996-4003.1990.
Tumor necrosis factors alpha and beta (TNF-alpha and TNF-beta) are multifaceted polypeptide cytokines which may mediate some of the significant changes in cellular homeostasis which accompany the invasion of the mammalian host by viruses, bacteria, and parasites. Although it is well established that bacterial lipopolysaccharide is a potent inducer of TNF-alpha, there is still very little known of the types of agents which can trigger the production of TNFs in mononuclear leukocytes. Using an enzyme-linked immunosorbent assay for measuring TNF-alpha and TNF-beta, we examined the capacity of various T-lymphocyte and beta-lymphocyte mitogens as well as microbial components to stimulate production of these cytokines in culture. The mitogens phytohemagglutinin, concanavalin A, and pokeweed mitogen induced production of both TNF-alpha and TNF-beta, while whole-killed Staphylococcus aureus and Bordetella pertussis, like lipopolysaccharide, were potent inducers of TNF-alpha but failed to stimulate TNF-beta production. TNF-alpha production was detectable within 1 h after stimulation, while TNF-beta production was not detected until after 8 h of culture. The bacterial products tetanus toxoid, purified protein derivative, pertussis filamentous hemagglutinin, and pertussis toxin were all able to induce TNF-alpha and TNF-beta production. Disrupted (frozen-thawed) Plasmodium falciparum-infected erythrocytes were also potent inducers of TNF-alpha and TNF-beta. The results demonstrated that a wide variety of microbial components are inducers of TNF-alpha. Some may not only be more effective than lipopolysaccharide but can also induce TNF-beta production. Furthermore, evidence is presented showing that TNF-beta but not TNF-alpha production correlates with lymphoproliferation.
肿瘤坏死因子α和β（TNF-α和TNF-β）是多方面的多肽细胞因子，它们可能介导了一些细胞稳态的显著变化，这些变化伴随着病毒、细菌和寄生虫对哺乳动物宿主的侵袭。虽然细菌脂多糖是TNF-α的有效诱导剂这一点已得到充分证实，但对于能够触发单核白细胞中TNF产生的试剂类型仍知之甚少。我们使用酶联免疫吸附测定法来测量TNF-α和TNF-β，检测了各种T淋巴细胞和B淋巴细胞有丝分裂原以及微生物成分在培养物中刺激这些细胞因子产生的能力。有丝分裂原植物血凝素、刀豆球蛋白A和商陆有丝分裂原可诱导TNF-α和TNF-β的产生，而全灭活的金黄色葡萄球菌和百日咳博德特氏菌，与脂多糖一样，是TNF-α的有效诱导剂，但不能刺激TNF-β的产生。刺激后1小时内可检测到TNF-α的产生，而TNF-β的产生直到培养8小时后才被检测到。细菌产物破伤风类毒素、纯化蛋白衍生物、百日咳丝状血凝素和百日咳毒素都能够诱导TNF-α和TNF-β的产生。破裂（冻融）的恶性疟原虫感染的红细胞也是TNF-α和TNF-β的有效诱导剂。结果表明，多种微生物成分都是TNF-α的诱导剂。有些不仅可能比脂多糖更有效，还能诱导TNF-β的产生。此外，有证据表明TNF-β而非TNF-α的产生与淋巴细胞增殖相关。
