Hahon N, Booth J A
J Interferon Res. 1984;4(1):17-27. doi: 10.1089/jir.1984.4.17.
Mammalian (LLC-MK2) cell monolayers pretreated with either chromium or manganese particles depressed viral induction of IFN by approximately 50% but the presence of metal particles did not prevent exogenous IFN from conferring antiviral cellular resistance. Manganese particles were more detrimental to viral IFN induction than chromium particles in that almost tenfold less of the former achieved a comparable magnitude of IFN inhibition. Although rates of influenza virus multiplication in either chromium or manganese-treated and control cell cultures were similar, virus attained a level of growth almost twofold higher in metal-treated cells than in controls. This was related to suppression of viral IFN induction by metal particles. Neuraminidase treatment of cell surface salioglycoproteins or pretreatment of chromium or manganese particles with sialic acid abrogated the adverse activity of metal particles on viral IFN induction. These findings suggest that the receptivity and interaction of cell membrane-bound sialic acid residues with metal particles are involved in the altered cellular protective response described.
用铬或锰颗粒预处理的哺乳动物(LLC-MK2)细胞单层可使病毒诱导的干扰素降低约50%,但金属颗粒的存在并不妨碍外源性干扰素赋予细胞抗病毒抗性。锰颗粒对病毒干扰素诱导的损害比铬颗粒更大,因为前者达到可比干扰素抑制程度所需的量几乎少了十倍。尽管在铬或锰处理的细胞培养物以及对照细胞培养物中流感病毒的增殖速率相似,但在金属处理的细胞中病毒达到的生长水平几乎比对照高两倍。这与金属颗粒对病毒干扰素诱导的抑制有关。用神经氨酸酶处理细胞表面唾液糖蛋白或用唾液酸预处理铬或锰颗粒可消除金属颗粒对病毒干扰素诱导的不利活性。这些发现表明,细胞膜结合的唾液酸残基与金属颗粒的接受性和相互作用参与了所述的细胞保护反应改变。