Department of Microbiology and Immunology, University of Arkansas for Medical Sciences and Arkansas Children's Hospital Research Institute, Little Rock, AR 72202, USA.
Infect Immun. 2011 Aug;79(8):3291-301. doi: 10.1128/IAI.00200-11. Epub 2011 May 16.
We utilized a recently developed model of intracervical infection with Chlamydia muridarum in the mouse to elicit a relatively synchronous infection during the initial developmental cycle in order to examine at the ultrastructural level the development of both the chlamydial inclusion and the onset of the inflammatory response. At 18 h after infection, only a few elementary bodies attached to cells were visible, as were an occasional intracellular intermediate body and reticulate body. By 24 h, inclusions had 2 to 5 reticulate bodies and were beginning to fuse. A few polymorphonuclear leukocytes (PMNs) were already present in the epithelium in the vicinity of and directly adjacent to infected cells. By 30 h, the inclusions were larger and consisted solely of reticulate bodies, but by 36 to 42 h, they contained intermediate bodies and elementary bodies as well. Many PMNs were adjacent to or actually inside infected cells. Chlamydiae appeared to exit the cell either (i) through disintegration of the inclusion membrane and rupture of the cell, (ii) by dislodgement of the cell from the epithelium by PMNs, or (iii) by direct invasion of the infected cell by the PMNs. When PMNs were depleted, the number of released elementary bodies was significantly greater as determined both visually and by culture. Interestingly, depletion of PMNs revealed the presence of inclusions containing aberrant reticulate bodies, reminiscent of effects seen in vitro when chlamydiae are incubated with gamma interferon. In vivo evidence for the contact-dependent development hypothesis, a potential mechanism for triggering the conversion of reticulate bodies to elementary bodies, and for translocation of lipid droplets into the inclusion is also presented.
我们利用新近开发的鼠型子宫颈感染沙眼衣原体模型，在初始发育周期中引发相对同步的感染，以便在超微结构水平上检查衣原体包涵体的发育和炎症反应的开始。感染后 18 小时，仅可见少数附着在细胞上的始体，偶尔还可见胞内中间体和网状体。24 小时时，包涵体中已有 2 至 5 个网状体，并开始融合。少数多形核白细胞（PMN）已经出现在受感染细胞附近和直接相邻的上皮细胞中。30 小时时，包涵体变大，仅包含网状体，但在 36 至 42 小时时，它们也包含中间体和始体。许多 PMN 紧邻或实际上位于感染细胞内。衣原体似乎通过以下几种方式离开细胞：（i）通过包涵体膜的崩解和细胞破裂，（ii）通过 PMN 将细胞从上皮细胞上逐出，或（iii）通过 PMN 直接入侵受感染的细胞。当 PMN 被耗尽时，通过肉眼观察和培养确定，释放的始体数量明显增加。有趣的是，耗尽 PMN 揭示了存在含有异常网状体的包涵体，这让人联想到在体外孵育衣原体时，当衣原体与γ干扰素孵育时观察到的效果。体内证据也表明了接触依赖性发育假说的存在，这是触发网状体转化为始体以及将脂滴转运到包涵体中的潜在机制。
