Parasites & vectors · 2013
Characterization of mouse brain microRNAs after infection with cyst-forming Toxoplasma gondii.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Xu Min-Jun, Zhou Dong-Hui, Nisbet Alasdair J, Huang Si-Yang, Fan Yi-Fan, Zhu Xing-Quan
Аннотация
BACKGROUND: The obligate intracellular parasite Toxoplasma gondii can interfere with host cell signaling pathways, alter host defense systems and cell cycle control, and establish a chronic infection in the central nervous system. T. gondii infection may alter the expression profile of host microRNAs (miRNAs) which have key regulatory functions at the post-transcriptional level.
METHODS: Using high-throughput sequencing and real-time quantitative PCR technology, we compared the miRNA expression profiles of uninfected mouse brains with brains from mice at 14 days and 21 days after infection with cyst-forming T. gondii (Type II).
RESULTS: A total of 51.30 million raw reads were obtained from all samples and 495 (14d infected mouse sample), 511 (14d sham-infected control), 504 (21d infected mouse sample) and 514 (21d sham-infected control) miRNA candidates identified. Among these, 414 miRNAs were consistent across all the studied groups, 17 were specific to the 14d infected group and 32 were specific to the 21d infected group. In addition, 9 miRNAs were common to both the 14d- and 21d-infected groups. Enrichment analysis for the targets of these miRNAs showed a high percentage of "protein tag" functions. Immune related targets including chemokines, cytokines, growth factors and interleukins were also found.
CONCLUSIONS: These results not only showed that the miRNA expression of the host can be changed by the invasion of cyst-forming T. gondii, but also indicated that the host attempts to respond using two tactics: marking proteins with "protein tags" and adaptation of immune related systems.
METHODS: Using high-throughput sequencing and real-time quantitative PCR technology, we compared the miRNA expression profiles of uninfected mouse brains with brains from mice at 14 days and 21 days after infection with cyst-forming T. gondii (Type II).
RESULTS: A total of 51.30 million raw reads were obtained from all samples and 495 (14d infected mouse sample), 511 (14d sham-infected control), 504 (21d infected mouse sample) and 514 (21d sham-infected control) miRNA candidates identified. Among these, 414 miRNAs were consistent across all the studied groups, 17 were specific to the 14d infected group and 32 were specific to the 21d infected group. In addition, 9 miRNAs were common to both the 14d- and 21d-infected groups. Enrichment analysis for the targets of these miRNAs showed a high percentage of "protein tag" functions. Immune related targets including chemokines, cytokines, growth factors and interleukins were also found.
CONCLUSIONS: These results not only showed that the miRNA expression of the host can be changed by the invasion of cyst-forming T. gondii, but also indicated that the host attempts to respond using two tactics: marking proteins with "protein tags" and adaptation of immune related systems.