Ultrastructural analysis of chlamydial antigen-containing vesicles everting from the Chlamydia trachomatis inclusion
Ultrastructural analysis of chlamydial antigen-containing vesicles everting from the Chlamydia trachomatis inclusion
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DOI：
10.1016/j.micinf.2006.01.018
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发表时间：
2006-05-01
影响因子：
5.8
通讯作者：
Wyrick, Priscilla B.
中科院分区：
文献类型：
--
作者：
Giles, David K.;Whittimore, Judy D.;Wyrick, Priscilla B.
在72-96小时发育周期结束时假定自然释放之前，已在受感染的上皮细胞胞浆和宿主细胞表面检测到几种衣原体抗原。这些额外包含抗原被认为可以影响重要的宿主细胞功能、抗原运输和呈递，并最终导致长期的炎症反应。为了开始剖析这些抗原从衣原体包涵体中逃逸的机制，这些抗原在接触抗生素后会增强，用沙眼衣原体血清型 E 感染极化子宫内膜上皮细胞 (HEC-1B) 36 小时或 48 小时。然后将感染的细胞暴露于体外未负载或预负载抗生素阿奇霉素的趋化人多形核中性粒细胞。通过电子显微镜观察，阿奇霉素介导的衣原体杀灭涉及衣原体外膜起泡的增加，随后在较大囊泡中出现大泡（i）从包涵体外翻但仍与包涵体相关，以及（ii）包涵体外部。通过包涵膜蛋白 A、F 和 G 在囊泡膜上的免疫定位，证明囊泡起源于衣原体包涵体膜。衣原体热休克蛋白 60 (chsp60) 拷贝 2 和 3，但不是拷贝 1，从 RB 中释放出来，并掺入外翻的包涵膜囊泡中，并递送到受感染的细胞表面。这些数据代表了一种早期抗原递送机制的直接证据，尽管是膜结合的，但超出了衣原体包涵体的范围。 (c) 2006 年爱思唯尔 SAS。版权所有。
Several chlamydial antigens have been detected in the infected epithelial cell cytosol and on the host cell surface prior to their presumed natural release at the end of the 72-96 h developmental cycle. These extra-inclusion antigens are proposed to influence vital host cell functions, antigen trafficking and presentation and, ultimately, contribute to a prolonged inflammatory response. To begin to dissect the mechanisms for escape of these antigens from the chlamydial inclusion, which are enhanced on exposure to antibiotics, polarized endometrial epithelial cells (HEC-1B) were infected with Chlamyclia trachomatis serovar E for 36 h or 48 h. Infected cells were then exposed to chemotactic human polymorphonuclear neutrophils not loaded or pre-loaded in vitro with the antibiotic azithromycin. Viewed by electron microscopy, the azithromycin-mediated killing of chlamydiae involved an increase in chlamydial outer membrane blebbing followed by the appearance of the blebs in larger vesicles (i) everting from but still associated with the inclusion as well as (ii) external to the inclusion. Evidence that the vesicles originated from the chlamydial inclusion membrane was shown by immuno-localization of inclusion membrane proteins A, F, and G on the vesicular membranes. Chlamydial heat shock protein 60 (chsp60) copies 2 and 3, but not copy 1, were released from RB and incorporated into the everted inclusion membrane vesicles and delivered to the infected cell surface. These data represent direct evidence for one mechanism of early antigen delivery, albeit membrane-bound, beyond the confines of the chlamydial inclusion. (c) 2006 Elsevier SAS. All rights reserved.