The Contribution of MicroRNA-182 in Genital Chlamydia trachomatis Infection

MicroRNA-182在生殖器沙眼衣原体感染中的作用

• 批准号: 9318447
• 负责人: Bernard Pragash Arulanandam
• 金额: $ 7.35万
• 依托单位: UNIVERSITY OF TEXAS SAN ANTONIO
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-07-14 至 2019-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9318447
• 关键词: Antigens; Bacterial Sexually Transmitted Diseases; Binding; C57BL/6 Mouse; CD4 Positive T Lymphocytes; Cell Culture Techniques; Cells; Chlamydia Infections; Chlamydia muridarum; Chlamydia trachomatis; Computer Simulation; Consensus; Data; Down-Regulation; Female; Genes; Genital system; Glycoproteins; Growth; Immune; Immunity; Immunization; Immunotherapy; In Vitro; Inbred BALB C Mice; Incidence; Infection; Inflammatory; Integration Host Factors; Interferon Type II; Interferons; Knowledge; Mass Spectrum Analysis; Mediating; MicroRNAs; Molecular; Mus; Pathology; Peptide Hydrolases; Preventive vaccine; Process; Proteins; RNA; Recombinants; Regulation; Reporting; Reproductive Biology; Role; Sexually Transmitted Diseases; Testing; Untranslated RNA; Up-Regulation; Vaccinated; Vaccination; Vaccines; alpha-Fetoproteins; bench to bedside; biological adaptation to stress; decorin; design; improved; in vivo; insight; knock-down; novel; protein expression; public health relevance; reproductive tract; spatiotemporal; vaccination strategy; vaccine candidate

DESCRIPTION (provided by applicant) Chlamydia trachomatis (Ct), is the leading cause of bacterial sexually transmitted infections in the U.S., with increasing incidence rates over the las 10-15 years. A bench-to-bedside solution for a preventative vaccine for Ct is not available. Knowledge of inherent host molecular mechanisms that may influence host immunity will be helpful in improving down-selection of "putative" anti-Ct vaccine candidate(s). To this end, there is growing consensus on the role of small non-coding species of regulatory RNA, i.e. microRNAs (miRs) in critical processes including immunity and reproductive biology. Additionally, vaccination strategies or immunotherapy using miRs have now been established. Our recent report on the role of miR modulating host immunity and association studies on Ct-miR(s) collectively highlight the importance of these immune modulators in Ct infections and underscores the need to define their contribution in anti-Ct immunity. In this proposal, we plan to investigate specifically, the role of miR-182 in colonization of Chlamydia muridarum (Cm) via regulation of host protein, Alpha-2HS-Glycoprotein (AHSG) in the murine genital tract. Additionally, we plan to investigate the regulation of miR-182-AHSG in vaccinated mice where antigen (Ag)-specific CD4+T cells and interferon-γ (IFN-γ) in accelerate Cm clearance from the genital tract. Taken together, this application aims at providing novel information on the role of miR-182 in chlamydial infections and modulation of miR-182 and its host targets by anti-Ct immunity.

描述（由申请人提供） 沙眼衣原体 (Ct) 是美国细菌性传播感染的主要原因，其发病率在过去 10-15 年间不断增加。目前还没有针对 Ct 预防性疫苗的从实验室到临床的解决方案。了解可能影响宿主免疫的固有宿主分子机制将有助于改善“假定的”抗 Ct 候选疫苗的向下选择。为此，人们对小型非编码调节RNA（即微小RNA（miR））在包括免疫和生殖生物学在内的关键过程中的作用达成了越来越多的共识。此外，现在已经建立了使用 miR 的疫苗接种策略或免疫疗法。我们最近关于 miR 调节宿主免疫作用的报告以及对 Ct-miR 的关联研究共同强调了这些免疫调节剂在 Ct 感染中的重要性，并强调需要确定它们在抗 Ct 免疫中的贡献。在本提案中，我们计划具体研究 miR-182 通过调节小鼠生殖道中的宿主蛋白 Alpha-2HS-糖蛋白 (AHSG) 在鼠衣原体 (Cm) 定植中的作用。此外，我们计划研究疫苗接种小鼠中 miR-182-AHSG 的调节，其中抗原 (Ag) 特异性 CD4+T 细胞和干扰素-γ (IFN-γ) 加速 Cm 从生殖道的清除。总而言之，本申请旨在提供有关 miR-182 在衣原体感染中的作用以及通过抗 Ct 免疫调节 miR-182 及其宿主靶标的新信息。

项目成果

Chlamydia and Its Many Ways of Escaping the Host Immune System.

衣原体及其逃避宿主免疫系统的多种方法。

• DOI: 10.1155/2019/8604958
• 发表时间: 2019
• 期刊: Journal of pathogens
• 影响因子: 2.6
• 作者: Wong,WonFen;Chambers,JamesP;Gupta,Rishein;Arulanandam,BernardP
• 通讯作者: Arulanandam,BernardP

A modified method for rapid quantification of Chlamydia muridarum using Fluorospot.

使用 Fluorospot 快速定量鼠衣原体的改进方法。

• DOI: 10.1016/j.mex.2019.08.005
• 发表时间: 2019
• 期刊: MethodsX
• 影响因子: 1.9
• 作者: Keck,Jonathon;Chambers,JamesP;Forsthuber,Thomas;Gupta,Rishein;Arulanandam,BernardP
• 通讯作者: Arulanandam,BernardP