کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5592181 | 1570711 | 2017 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Streptococcus gordonii induces nitric oxide production through its lipoproteins stimulating Toll-like receptor 2 in murine macrophages
ترجمه فارسی عنوان
استرپتوکوک گوردونی، تولید اکسید نیتریک را از طریق لیپوپروتئین های آن تحریک کننده گیرنده 2 مانند تومور در ماکروفاژهای ماکروفاژ
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
چکیده انگلیسی
Streptococcus gordonii, a Gram-positive commensal in the oral cavity, is an opportunistic pathogen that can cause endodontic and systemic infections resulting in infective endocarditis. Lipoteichoic acid (LTA) and lipoprotein are major virulence factors of Gram-positive bacteria that are preferentially recognized by Toll-like receptor 2 (TLR2) on immune cells. In the present study, we investigated the effect of S. gordonii LTA and lipoprotein on the production of the representative inflammatory mediator nitric oxide (NO) by the mouse macrophages. Heat-killed S. gordonii wild-type and an LTA-deficient mutant (ÎltaS) but not a lipoprotein-deficient mutant (Îlgt) induced NO production in mouse primary macrophages and the cell line, RAW 264.7. S. gordonii wild-type and ÎltaS also induced the expression of inducible NO synthase (iNOS) at the mRNA and protein levels. In contrast, the Îlgt mutant showed little effect under the same condition. Furthermore, S. gordonii wild-type and ÎltaS induced NF-κB activation, STAT1 phosphorylation, and IFN-β expression, which are important for the induction of iNOS gene expression, with little activation by Îlgt. S. gordonii wild-type and ÎltaS showed an increased adherence and internalization to RAW 264.7 cells compared to Îlgt. In addition, S. gordonii wild-type and ÎltaS, but not Îlgt, substantially increased TLR2 activation while none of these induced NO production in TLR2-deficient macrophages. Triton X-114-extracted lipoproteins from S. gordonii were sufficient to induce NO production. Collectively, we suggest that lipoprotein is an essential cell wall component of S. gordonii to induce NO production in macrophages through TLR2 triggering NF-κB and STAT1 activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 82, February 2017, Pages 75-83
Journal: Molecular Immunology - Volume 82, February 2017, Pages 75-83
نویسندگان
Hyun Young Kim, Jung Eun Baik, Ki Bum Ahn, Ho Seong Seo, Cheol-Heui Yun, Seung Hyun Han,