کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10941173 | 1095617 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Local delivery of soluble interleukin-6 receptors to improve the outcome of alpha-toxin producing Staphylococcus aureus infection in mice
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کلمات کلیدی
NF-κBTNFPLFMCPsIL-6R - SIL-6RSTAT - آمارStaphylococcus aureus - استافیلوکوک اورئوسS. aureus - استافیلوکوکوس اورئوسStaphylococcus - استافیلوکوکهاinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینEnzyme-linked immunosorbent assay - تست الیزاELISA - تست الیزاtumor necrosis factor - فاکتور نکروز تومورnuclear factor κB - فاکتور هسته ای κBSignal transducer and activator of transcription - مبدل سیگنال و فعال کننده رونویسیmonocyte chemoattractant protein - پروتئین شیمیایی monocyte chemoattractantInterleukin-6 receptor - گیرنده اینترلوکین -6Soluble IL-6 receptor - گیرنده حلقوی IL-6
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Local delivery of soluble interleukin-6 receptors to improve the outcome of alpha-toxin producing Staphylococcus aureus infection in mice Local delivery of soluble interleukin-6 receptors to improve the outcome of alpha-toxin producing Staphylococcus aureus infection in mice](/preview/png/10941173.png)
چکیده انگلیسی
Staphylococcal alpha-toxin enhances interleukin (IL)-6 secretion in mice infected with Staphylococcus aureus. The role of alpha-toxin-induced IL-6 secretion in host defense has not been sufficiently clarified. In the present study, IL-6 signaling was transiently regulated using soluble IL-6 receptors (sIL-6R) to investigate the role of IL-6 in the early stage of abdominal S. aureus infection. In mice challenged with bacteria producing high alpha-toxin levels, the local delivery of sIL-6R was effective in improving the survival rate, the resolution of neutrophilia and the bacteria clearance. Mice that had received sIL-6R and survived showed high levels of IL-6, monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-alpha. In contrast, mice that died in spite of the delivery of sIL-6R showed high levels of interferon (IFN)-gamma and IL-1alpha and low TNF-alpha level. When the effect of soluble gp130, a sIL-6R antagonist, was examined, the number of neutrophils increased significantly and the MCP-1 level decreased significantly, compared to the group that received sIL-6R alone; the number of viable bacteria also tended to increase as a result of the inhibition of IL-6 signaling. The cellular phosphotyrosine level in alpha-toxin-treated macrophages was reduced in cultures supplemented with recombinant IL-6 in vitro. These results suggest that IL-6 enhances bactericidal activity and reduces the number of immune cells that are activated abnormally through the regulation of inflammatory cytokines during the early stage of infection in alpha-toxin producers.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 209, Issue 9, 15 March 2005, Pages 651-660
Journal: Immunobiology - Volume 209, Issue 9, 15 March 2005, Pages 651-660
نویسندگان
Tsuyoshi Onogawa,