کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6135706 | 1224889 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA fragments derived from Streptococcus pyogenes enable activation of neutrophil phagocytosis: in vitro study
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
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چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbes and Infection - Volume 15, Issue 3, March 2013, Pages 212-218
Journal: Microbes and Infection - Volume 15, Issue 3, March 2013, Pages 212-218
نویسندگان
Taiji Ogawa, Yutaka Terao, Mariko Honda-Ogawa, Sakae Hashimoto, Kazunori Ikebe, Yoshinobu Maeda, Shigetada Kawabata,