Chlamydia trachomatis responds to heat shock, penicillin induced persistence, and IFN-gamma persistence by altering levels of the extracytoplasmic stress response protease HtrA.

Chlamydia trachomatis responds to heat shock, penicillin induced persistence, and IFN-gamma persistence by altering levels of the extracytoplasmic stress response protease HtrA.
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DOI:
10.1186/1471-2180-8-190
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发表时间:
2008-11-06
期刊:
影响因子:
4.2
通讯作者:
Timms P
Timms P
中科院分区:
生物学3区
文献类型:
--
作者:
Huston WM;Theodoropoulos C;Mathews SA;Timms P

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沙眼衣原体是一种专性细胞内病原体,是世界范围内最普遍的细菌性性传播感染,也是可预防性失明的主要原因。HtrA是在许多细菌中发现的毒力和应激反应周质丝氨酸蛋白酶和分子伴侣。重组纯化C.沙眼衣原体HtrA先前已显示具有这两种活性。本研究探讨了沙眼衣原体HtrA的生理作用。沙眼衣原体htrA基因补充了大肠杆菌htrA-(>42°C)的致死高温表型。在衣原体热休克实验中,通过免疫印迹和免疫荧光检测到HtrA水平增加。共聚焦激光扫描显微镜显示可能的周质定位的HtrA。在青霉素诱导的沙眼衣原体的持久性,HtrA水平(作为LPS的比例)最初低于对照急性培养物(感染后20小时),但增加到超过急性培养物在感染后44小时。这与观察到较低水平的HtrA的IFN-γ持久性不同,表明沙眼衣原体IFN-γ持久性不涉及广泛的应激反应。异源热休克保护大肠杆菌,并增加HtrA细胞壁破坏期间通过青霉素和热休克,表明HtrA在高蛋白应激条件下的沙眼衣原体的重要作用。
Chlamydia trachomatis, an obligate intracellular human pathogen, is the most prevalent bacterial sexually transmitted infection worldwide and a leading cause of preventable blindness. HtrA is a virulence and stress response periplasmic serine protease and molecular chaperone found in many bacteria. Recombinant purified C. trachomatis HtrA has been previously shown to have both activities. This investigation examined the physiological role of Chlamydia trachomatis HtrA. The Chlamydia trachomatis htrA gene complemented the lethal high temperature phenotype of Escherichia coli htrA- (>42°C). HtrA levels were detected to increase by western blot and immunofluorescence during Chlamydia heat shock experiments. Confocal laser scanning microscopy revealed a likely periplasmic localisation of HtrA. During penicillin induced persistence of Chlamydia trachomatis, HtrA levels (as a ratio of LPS) were initially less than control acute cultures (20 h post infection) but increased to more than acute cultures at 44 h post infection. This was unlike IFN-γ persistence where lower levels of HtrA were observed, suggesting Chlamydia trachomatis IFN-γ persistence does not involve a broad stress response. The heterologous heat shock protection for Escherichia coli, and increased HtrA during cell wall disruption via penicillin and heat shock, indicates an important role for HtrA during high protein stress conditions for Chlamydia trachomatis.
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