While glycogen synthase A deficiency can reduce the growth and proliferation of Chlamydia muridarum, the effect of glycogen synthase A on the pathogenic process of C. muridarum remains unclear. To characterize the effect of glycogen synthase A deficiency on the pathogenicity of C. muridarum in the genital tract, BALB/c mice were intravaginally inoculated with wild-type, plasmid-free and glycogen synthase A-deficient C. muridarum, and the genital tract tissue was isolated to assess the severity of hydrosalpinx and the levels of oviduct dilatation at day 60 after infection. The glycogen storage capacity and in vitro infection ability of different C. muridarum strains were analyzed by periodic acid-Schiff staining and quantification of progeny elementary body(EB) formation. The tissue homogenate was used to determine the recovery of different C. muridarum strains. The results show that glycogen synthase A-deficient C. muridarum induced reduction of hydrosalpinx and attenuated the extent of oviduct dilatation in mice, and exhibited reduced growth and proliferation in the mouse lower genital tract. In addition, glycogen synthase A point mutations at different sites reduced the glycogen storage capacity and in vitro infectivity of C. muridarum to different degrees. Glycogen synthase A deficiency also reduced the host inflammatory reaction and ascending infection of C. muridarum.

译文

虽然糖原合酶A缺乏可以减少衣原体的生长和增殖,但糖原合酶A对C. muridarum的致病过程的影响尚不清楚。为了表征糖原合酶A缺乏对生殖道C. muridarum致病性的影响,将BALB/c小鼠阴道内接种野生型,无质粒和糖原合酶A缺陷的C. muridarum,并在感染后第60天分离生殖道组织以评估输卵管积水的严重程度和输卵管扩张水平。通过高碘酸-席夫染色和子代基本体 (EB) 形成的定量分析了不同muridarum菌株的糖原储存能力和体外感染能力。组织匀浆用于确定不同的C. muridarum菌株的回收率。结果表明,糖原合酶A缺乏的C. muridarum可诱导小鼠输卵管积水的减少并减弱输卵管扩张的程度,并在小鼠下生殖道中表现出减少的生长和增殖。此外,不同位点的糖原合酶A点突变不同程度地降低了C. muridarum的糖原储存能力和体外感染性。糖原合酶A缺乏症还减少了宿主的炎症反应和C. muridarum的上升感染。

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