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由[具体名称]膜泡诱导的肠上皮细胞转录组反应 。(原文中“.”处信息缺失,翻译只能到此程度)

Transcriptome responses of intestinal epithelial cells induced by membrane vesicles of .

作者信息

Karthikeyan Raman, Gayathri Pratapa, Ramasamy Subbiah, Suvekbala Vemparthan, Jagannadham Medicharla V, Rajendhran Jeyaprakash

机构信息

Department of Genetics, School of Biological Sciences, Madurai Kamaraj University, Madurai, 625021, Tamil Nadu, India.

CSIR - Centre for Cellular and Molecular Biology, Tarnaka, Hyderabad 500007, India.

出版信息

Curr Res Microb Sci. 2023 Mar 6;4:100185. doi: 10.1016/j.crmicr.2023.100185. eCollection 2023.

Abstract

Membrane vesicles (MVs) serve as an essential virulence factor in several pathogenic bacteria. The release of MVs by is only recently recognized; still, the enigmatic role of MVs in pathogenesis is yet to be established. We report the transcriptome response of Caco-2 cells upon exposure to MVs and the L. that leads to observe the up-regulation of autophagy-related genes in the early phase of exposure to MVs. Transcription of inflammatory cytokines is to the peak at the fourth hour of exposure. An array of differentially expressed genes was associated with actin cytoskeleton rearrangement, autophagy, cell cycle arrest, and induction of oxidative stress. At a later time point, transcriptional programs are generated upon interaction with MVs to evade innate immune signals, by modulating the expression of anti-inflammatory genes. KEGG pathway analysis is palpably confirming that MVs appear principally responsible for the induction of immune signaling pathways. Besides, MVs induced the expression of cell cycle regulatory genes, likely responsible for the ability to prolong host cell survival, thus protecting the replicative niche for L. . Notably, we identified several non-coding RNAs (ncRNAs), possibly involved in the regulation of early manipulation of the host gene expression, essential for the persistence of L. .

摘要

膜泡(MVs)是几种病原菌中一种重要的毒力因子。MVs的释放直到最近才被认识到;然而,MVs在发病机制中的神秘作用仍有待确定。我们报告了Caco-2细胞在暴露于MVs和导致在暴露于MVs的早期观察到自噬相关基因上调的情况下的转录组反应。炎性细胞因子的转录在暴露后第四小时达到峰值。一系列差异表达基因与肌动蛋白细胞骨架重排、自噬、细胞周期停滞和氧化应激诱导有关。在稍后的时间点,与MVs相互作用时会产生转录程序,通过调节抗炎基因的表达来逃避先天免疫信号。KEGG通路分析明显证实MVs似乎主要负责免疫信号通路的诱导。此外,MVs诱导了细胞周期调节基因的表达,这可能是延长宿主细胞存活能力的原因,从而为提供复制生态位。值得注意的是,我们鉴定了几种非编码RNA(ncRNAs),它们可能参与宿主基因表达早期调控的调节,这对的持续存在至关重要。 (原文中“L.”表述不完整,可能影响部分理解)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b6/10023947/2722424bd8a5/ga1.jpg

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