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Sca2 和 RickA 在帕克氏立克次体在斑点钝缘蜱中的传播中的作用。

Role of Sca2 and RickA in the Dissemination of Rickettsia parkeri in Amblyomma maculatum.

机构信息

Vector-Borne Disease Laboratories, Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana, USA.

Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, California, USA.

出版信息

Infect Immun. 2018 May 22;86(6). doi: 10.1128/IAI.00123-18. Print 2018 Jun.

Abstract

The Gram-negative obligate intracellular bacterium is an emerging tick-borne human pathogen. Recently, Sca2 and RickA have been implicated in adherence and actin-based motility in vertebrate host cell infection models; however, the rickettsia-derived factors essential to tick infection are unknown. Using mutants lacking functional Sca2 or RickA to compare actin polymerization, replication, and cell-to-cell spread , similar phenotypes in tick and mammalian cells were observed. Specifically, actin polymerization in cultured tick cells is controlled by the two separate proteins in a time-dependent manner. To assess the role of Sca2 and RickA in dissemination in the tick host, -free , the natural vector of , was exposed to wild-type, ::, or :: bacteria, and individual tick tissues, including salivary glands, midguts, ovaries, and hemolymph, were analyzed at 12 h and after continued bloodmeal acquisition for 3 or 7 days postexposure. Initially, ticks exposed to wild-type had the highest rickettsial load across all organs; however, rickettsial loads decreased and wild-type rickettsiae were cleared from the ovaries at 7 days postexposure. In contrast, ticks exposed to :: or :: had comparatively lower rickettsial loads, but bacteria persisted in all organs for 7 days. These data suggest that while RickA and Sca2 function in actin polymerization in tick cells, the absence of these proteins did not change dissemination patterns within the tick vector.

摘要

革兰氏阴性专性细胞内细菌是一种新兴的蜱传人类病原体。最近,Sca2 和 RickA 被牵连到脊椎动物宿主细胞感染模型中的粘附和肌动蛋白基础运动中;然而,蜱感染所必需的立克次体衍生因子尚不清楚。使用缺乏功能性 Sca2 或 RickA 的 突变体来比较肌动蛋白聚合、复制和细胞间传播,在蜱和哺乳动物细胞中观察到类似的表型。具体来说,培养的蜱细胞中的肌动蛋白聚合受两种独立的蛋白质以时间依赖的方式控制。为了评估 Sca2 和 RickA 在蜱宿主传播中的作用,将 无 的天然载体暴露于野生型、:: 或 :: 细菌中,并在暴露后 12 小时以及继续吸血获取 3 或 7 天后分析单个蜱组织,包括唾液腺、中肠、卵巢和血淋巴。最初,暴露于野生型 的蜱在所有器官中的立克次体负荷最高;然而,立克次体负荷在暴露后 7 天下降,野生型立克次体从卵巢中清除。相比之下,暴露于 :: 或 :: 的蜱的立克次体负荷相对较低,但细菌在所有器官中持续存在 7 天。这些数据表明,虽然 RickA 和 Sca2 在蜱细胞中的肌动蛋白聚合中起作用,但这些蛋白质的缺失并没有改变蜱载体中的传播模式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/49f1/5964526/4e85fd73bb22/zii9990924180001.jpg

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