感染鹦鹉热衣原体的L细胞中对放线菌酮耐药的糖基化作用
Cycloheximide-resistant glycosylation in L cells infected with Chlamydia psittaci.
作者信息
Stokes G V
出版信息
Infect Immun. 1974 Mar;9(3):497-9. doi: 10.1128/iai.9.3.497-499.1974.
Abstract
L cells (mouse fibroblasts), uninfected and infected with the meningopneumonitis strain of Chlamydia psittaci, were labeled with [(14)C]glucosamine, and their membranous organelles were separated by isopycnic equilibrium centrifugation of whole cell homogenates on discontinuous sucrose gradients. Glycosylation of host membranes continued throughout the infection. Cycloheximide almost completely inhibited glycosylation in uninfected L cells, but it only partially inhibited the process in infected host cells. Cycloheximide-resistant glycosylation of membrane fractions with [(14)C]glucosamine increased as the infection proceeded and was probably due to the action of chlamydial enzymes. Modification of host membranes by glycosylation may play a role in the natural development of chlamydial infections.
摘要
用[¹⁴C]葡糖胺标记未感染以及感染了鹦鹉热衣原体脑膜肺炎菌株的L细胞（小鼠成纤维细胞），通过在不连续蔗糖梯度上对全细胞匀浆进行等密度平衡离心来分离其膜性细胞器。在整个感染过程中，宿主细胞膜的糖基化持续进行。放线菌酮几乎完全抑制未感染L细胞中的糖基化，但仅部分抑制感染宿主细胞中的这一过程。随着感染的进展，用[¹⁴C]葡糖胺进行的膜组分抗放线菌酮糖基化增加，这可能是衣原体酶作用的结果。通过糖基化对宿主细胞膜进行修饰可能在衣原体感染的自然发展中起作用。
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