lncRNA LINC00152 和 LARS2-AS1 的诊断价值及其在结核病巨噬细胞免疫反应中的调控作用

IF 2.8 3区 医学 Q3 IMMUNOLOGY
Wenlong Xu , Jihua Yang , Haizhen Yu , Shizhen Li
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引用次数: 0

摘要

方法 通过 qRT-PCR 检测 LINC00152 和 LARS2-AS1 在健康人、LTB 患者和 ATB 患者中的表达水平。构建 ROC 曲线以显示它们作为生物标记物的潜力。为了发现 LINC00152 和 LARS2-AS1 对 Mtb 感染的影响,还测定了 Mtb 细胞内存活试验和免疫相关细胞因子的水平。结果LINC00152和LARS2-AS1的水平在ATB和LTB患者以及Mtb感染的巨噬细胞中显著升高。LINC00152和LARS2-AS1能区分LTB和健康人,以及ATB和LTB。结论LINC00152和LARS2-AS1可被视为结核病的潜在生物标志物。LINC00152和LARS2-AS1具有抗结核的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Diagnostic value of lncRNAs LINC00152 and LARS2-AS1 and their regulatory roles in macrophage immune response in tuberculosis

Objectives

To determine the usefulness of LINC00152 and LARS2-AS1 as potential biomarkers for latent tuberculosis (LTB) and active tuberculosis (ATB), as well as their effect on Mycobacterium (Mtb) infection.

Methods

The expression levels of LINC00152 and LARS2-AS1 in the health, patients with LTB and ATB were detected by qRT-PCR. The ROC curves were constructed to show their potential as biomarkers. The intracellular survival assays for Mtb and the levels of immune-related cytokines were determined to discover the effect of LINC00152 and LARS2-AS1 on Mtb infection. The relationships of miR-485-5p with LINC00152 and LARS2-AS1 were explored.

Results

LINC00152 and LARS2-AS1 levels were significantly elevated in patients with ATB and LTB, and Mtb-infected macrophages. LINC00152 and LARS2-AS1 can distinguish the LTB from the health and ATB from LTB. LARS2-AS1 and LINC00152 knock-down reduced the intracellular Mtb survival and induced cellular immune response after Mtb challenge. miR-485-5p was a targeting miRNA for LINC00152 and LARS2-AS1.

Conclusions

LINC00152 and LARS2-AS1 can be considered as potential biomarkers for tuberculosis disease. LINC00152 and LARS2-AS1 have anti-Mtb effects.

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来源期刊
Tuberculosis
Tuberculosis 医学-呼吸系统
CiteScore
4.60
自引率
3.10%
发文量
87
审稿时长
49 days
期刊介绍: Tuberculosis is a speciality journal focusing on basic experimental research on tuberculosis, notably on bacteriological, immunological and pathogenesis aspects of the disease. The journal publishes original research and reviews on the host response and immunology of tuberculosis and the molecular biology, genetics and physiology of the organism, however discourages submissions with a meta-analytical focus (for example, articles based on searches of published articles in public electronic databases, especially where there is lack of evidence of the personal involvement of authors in the generation of such material). We do not publish Clinical Case-Studies. Areas on which submissions are welcomed include: -Clinical TrialsDiagnostics- Antimicrobial resistance- Immunology- Leprosy- Microbiology, including microbial physiology- Molecular epidemiology- Non-tuberculous Mycobacteria- Pathogenesis- Pathology- Vaccine development. This Journal does not accept case-reports. The resurgence of interest in tuberculosis has accelerated the pace of relevant research and Tuberculosis has grown with it, as the only journal dedicated to experimental biomedical research in tuberculosis.
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