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衣原体感染期间ATP水平和葡萄糖代谢的增强。活细胞的核磁共振研究。

Enhancement of ATP levels and glucose metabolism during an infection by Chlamydia. NMR studies of living cells.

作者信息

Ojcius D M, Degani H, Mispelter J, Dautry-Varsat A

机构信息

Unité de Biologie des Interactions Cellulaires, CNRS 1960, Institut Pasteur, Paris, France.

出版信息

J Biol Chem. 1998 Mar 20;273(12):7052-8. doi: 10.1074/jbc.273.12.7052.

Abstract

The Chlamydia species are obligate intracellular bacteria that proliferate only within the infected cell. Since the extracellular bacteria are metabolically inert and there are no cell-free systems for characterizing Chlamydia metabolism, we studied metabolic changes related to ATP synthesis and glycolysis in HeLa cells infected with Chlamydia psittaci during the course of the 2-day infection cycle using noninvasive 31P and 13C NMR methods. We find that the infection stimulates ATP synthesis in the infected cell, with a peak of ATP levels occurring midway through the infection cycle, when most of the metabolically active bacteria are proliferating. The infection also stimulates synthesis of glutamate with a similar time course as for ATP. The stimulation is apparently due to an enhancement in glucose consumption by the infected cell, which also results in an increased rate of lactate production and glutamate synthesis as well as higher glycogen accumulation during the infection. Concurrently, infection leads to an increase in the expression of the glucose transporter, GLUT-1, on HeLa cells, which may account for the enhanced glucose consumption. The chlamydiae are thus able to stimulate glucose transport in the host cell sufficiently to compensate for the extra energy load on the cell represented by the infection.

摘要

衣原体属是专性细胞内细菌,仅在受感染细胞内增殖。由于细胞外细菌代谢惰性,且不存在用于表征衣原体代谢的无细胞系统,我们使用非侵入性的³¹P和¹³C NMR方法,研究了在2天感染周期内感染鹦鹉热衣原体的HeLa细胞中与ATP合成和糖酵解相关的代谢变化。我们发现感染刺激了受感染细胞中的ATP合成,ATP水平在感染周期中期达到峰值,此时大多数代谢活跃的细菌正在增殖。感染还以与ATP相似的时间进程刺激谷氨酸的合成。这种刺激显然是由于受感染细胞葡萄糖消耗增加所致,这也导致感染期间乳酸生成率、谷氨酸合成增加以及糖原积累增多。同时,感染导致HeLa细胞上葡萄糖转运蛋白GLUT-1的表达增加,这可能解释了葡萄糖消耗的增加。因此,衣原体能够充分刺激宿主细胞中的葡萄糖转运,以补偿感染所代表的细胞额外能量负荷。

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