Wadee A A, Clara A M
School of Pathology, South African Institute for Medical Research, Johannesburg.
Infect Immun. 1989 Mar;57(3):864-9. doi: 10.1128/iai.57.3.864-869.1989.
This study examined the effects of a 25-kilodalton (kDa) glycolipoprotein derived from Mycobacterium tuberculosis on phagocyte functions associated with antimicrobial activity. The 25-kDa fraction inhibited the ability of both polymorphonuclear cells and cultured monocytes to release lysozyme and produce hydrogen peroxide. In addition, the glycolipoprotein was capable of reducing hexose monophosphate shunt activity and interfered with the ability of polymorphonuclear cells to reduce Nitro Blue Tetrazolium. Inhibition of these antimicrobial systems was optimal at a 50-micrograms/ml concentration of the 25-kDa fraction. Gamma interferon, but not alpha interferon, partially reversed the inhibitory effect of the mycobacterial component in all of the systems assessed. These studies indicate important mechanisms in the understanding of the pathogenesis of tuberculosis and suggest that gamma interferon may have a therapeutic role in mycobacterial diseases.
本研究检测了一种源自结核分枝杆菌的25千道尔顿(kDa)糖脂蛋白对与抗菌活性相关的吞噬细胞功能的影响。25 kDa组分抑制了多形核细胞和培养的单核细胞释放溶菌酶和产生过氧化氢的能力。此外,该糖脂蛋白能够降低磷酸己糖旁路活性,并干扰多形核细胞还原硝基蓝四唑的能力。在25 kDa组分浓度为50微克/毫升时,对这些抗菌系统的抑制作用最为显著。γ干扰素而非α干扰素能部分逆转该分枝杆菌成分在所有评估系统中的抑制作用。这些研究揭示了理解结核病发病机制的重要机制,并表明γ干扰素可能在分枝杆菌疾病中具有治疗作用。