Investigation of MicroRNA fragments derived from Streptococci
链球菌来源的 MicroRNA 片段的研究
基本信息
- 批准号:23890111
- 负责人:
- 金额:$ 1.83万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Research Activity Start-up
- 财政年份:2011
- 资助国家:日本
- 起止时间:2011 至 2012
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
MicroRNAs are single-stranded RNAs that regulate gene expression by forming imperfect base pairs, which have also been speculated to play regulatory roles in gene expression of Streptococcus pyogenes itself. We hypothesized that bacterial microRNAs cause molecular interference in host, when there is high homology to human microRNAs. Total RNA from cultured S. pyogenes strain SSI-1 was isolated and the cDNA fragments were then inserted into vector plasmid and transformed to competent cells, after which genomic sequence analyses were performed. Cell transfection, evaluation of mRNA transcription, measurement of inflammatory mediators, and assessment of surviving bacteria with murine splenocytes were also performed. Three microRNAs were selected from about 600 candidates according to their homology with human genome DNA. In the quantitative method, transcription of nasopharyngeal cells with microRNA was significantly lower in 2 of 11 targets, and greater in 10 of 11 targets. The ELISA findings revealed that transcription of MIP-2 was significantly greater with miR-SSI1-221 and miR-SSI1-281. Furthermore, strain SSI-1 had significantly higher survival in the supernatant of the control as compared to the miR-SSI1-221 and miR-SSI1-281 transfected cells. In conclusion, microRNA fragments derived from S. pyogenes have a high homology to the human genome and contribute to enhancement of the host immune system. 交
MicroRNAs are single-stranded RNAs that regulate gene expression by forming imperfect base pairs, which have also been speculated to play regulatory roles in gene expression of Streptococcus pyogenes itself. We hypothesized that bacterial microRNAs cause molecular interference in host, when there is high homology to human microRNAs. Total RNA from cultured S. pyogenes strain SSI-1 was isolated and the cDNA fragments were then inserted into vector plasmid and transformed to competent cells, after which genomic sequence analyses were performed. Cell transfection, evaluation of mRNA transcription, measurement of inflammatory mediators, and assessment of surviving bacteria with murine splenocytes were also performed. Three microRNAs were selected from about 600 candidates according to their homology with human genome DNA. In the quantitative method, transcription of nasopharyngeal cells with microRNA was significantly lower in 2 of 11 targets, and greater in 10 of 11 targets. The ELISA findings revealed that transcription of MIP-2 was significantly greater with miR-SSI1-221 and miR-SSI1-281. Furthermore, strain SSI-1 had significantly higher survival in the supernatant of the control as compared to the miR-SSI1-221 and miR-SSI1-281 transfected cells. In conclusion, microRNA fragments derived from S. pyogenes have a high homology to the human genome and contribute to enhancement of the host immune system. Hand in
项目成果
期刊论文数量(12)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Long-term survival of salivary streptococci on dental devices made of EVA.
唾液链球菌在 EVA 制成的牙科器械上长期存活。
- DOI:
- 发表时间:2012
- 期刊:
- 影响因子:0
- 作者:Ogawa;T.;Yamasaki;S.;Honda;M.;Terao;Y.;Kawabata;S.;and Maeda;Y.
- 通讯作者:Y.
Poor oral condition promotes harboring salivary pneumococcus in elderly.
口腔状况不佳会促进老年人唾液腺肺炎球菌的藏匿。
- DOI:
- 发表时间:2012
- 期刊:
- 影响因子:0
- 作者:Ogawa T;Kagawa R;Ikebe K;Honda M;Terao Y;Kawabata S;Maeda Y
- 通讯作者:Maeda Y
MicroRNA fragments derived from Streptococcus pyogenes enable activation of neutrophil phagocytosis : in vitro study
源自化脓性链球菌的 MicroRNA 片段能够激活中性粒细胞吞噬作用:体外研究
- DOI:10.1016/j.micinf.2012.11.009
- 发表时间:2013
- 期刊:
- 影响因子:5.8
- 作者:Ogawa T;Terao Y;Honda-Ogawa M;Hashimoto S;Ikebe K;Maeda Y;and Kawabata S
- 通讯作者:and Kawabata S
Clinically acceptable restorations may be a hotbed for cariogenic microbes
临床上可接受的修复体可能是致龋微生物的温床
- DOI:10.1111/j.1741-2358.2011.00571.x
- 发表时间:2011
- 期刊:
- 影响因子:2
- 作者:Ogawa T;Ikebe K;Murai S;Enoki K;Maeda Y;Imazato S;Ebisu S
- 通讯作者:Ebisu S
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