Shenker B J, DiRienzo J M
J Immunol. 1984 May;132(5):2357-62.
Fusobacterium nucleatum has been implicated in the pathogenesis of several diseases, including urinary tract infections, bacteremia, pericarditis, otitis media, and disorders of the oral cavity such as pulpal infections, alveolar bone abscesses, and periodontal disease. In this study, we examined sonic extracts of F. nucleatum strain FDC 364 for its ability to alter human lymphocyte function. We found that the soluble cytoplasmic fraction (CF) of the sonic extract was able to cause a dose-dependent inhibition of human lymphocyte responsiveness to Con A, PHA, PWM, and the recall antigen SKSD. Suppression involved altered DNA, RNA, and protein synthesis; there was no effect on cell viability. The suppressive activity is nondialyzable and heat labile. To achieve maximal suppression in 96-hr cell cultures, the CF had to be added to cells during the first 24 hr of incubation. Inhibition was reduced when the CF was added at 48 hr, and no suppression was observed when addition was at 72 or 96 hr (along with [3H]TdR). Furthermore, cells could be protected from the suppressive effects of the CF by washing within 24 hr of exposure. Suppression did not involve nonspecific effects on thymidine utilization. Although the mechanism of action of the F. nucleatum immunosuppressive activity has not yet been determined, we can rule out a requirement for monocytes/macrophages and activation of T suppressor cells. It has been proposed that impaired host defense may play a pivotal role in the pathogenesis of many diseases. The data presented in this paper suggest that local and/or systemic immunosuppression could be initiated by F. nucleatum. This immunosuppression may alter the nature and consequences of host-parasite interactions, thereby enhancing the pathogenicity of F. nucleatum itself or that of some other opportunistic organism.
具核梭杆菌与多种疾病的发病机制有关,包括尿路感染、菌血症、心包炎、中耳炎以及口腔疾病,如牙髓感染、牙槽骨脓肿和牙周病。在本研究中,我们检测了具核梭杆菌菌株FDC 364的超声提取物改变人淋巴细胞功能的能力。我们发现,超声提取物的可溶性细胞质部分(CF)能够对人淋巴细胞对刀豆蛋白A、植物血凝素、美洲商陆有丝分裂原和回忆抗原SKSD的反应产生剂量依赖性抑制。抑制作用涉及DNA、RNA和蛋白质合成的改变;对细胞活力没有影响。抑制活性不可透析且对热不稳定。为了在96小时的细胞培养中实现最大抑制,CF必须在培养的前24小时内添加到细胞中。当在48小时添加CF时,抑制作用减弱,而在72或96小时添加(与[3H]胸苷一起)时未观察到抑制作用。此外,在暴露后24小时内通过洗涤可使细胞免受CF的抑制作用。抑制作用不涉及对胸苷利用的非特异性影响。虽然具核梭杆菌免疫抑制活性的作用机制尚未确定,但我们可以排除单核细胞/巨噬细胞的需求和T抑制细胞的激活。有人提出,宿主防御受损可能在许多疾病的发病机制中起关键作用。本文提供的数据表明,具核梭杆菌可能引发局部和/或全身免疫抑制。这种免疫抑制可能会改变宿主-寄生虫相互作用的性质和后果,从而增强具核梭杆菌本身或其他一些机会性生物体的致病性。