کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9017301 | 1128340 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IL-1β induces IL-8 in bronchial cells via NF-κB and NF-IL6 transcription factors and can be suppressed by glucocorticoids
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
IKKECACCT helpergranulocyte-macrophage colony stimulating factorc-Jun N terminal kinaseRegulated upon Activation, Normal T cell Expressed and SecretedIL-8IL-1 receptor associated kinaseGM-CSFNF-κBAP-1GREERKRT-PCRPBSJnkCATIκB kinase - IkB kinaseMAPK - MAPKinterleukin - اینترلوکینLung - ریهnuclear factor - عامل هسته ایIRAK - عراقGlucocorticoid response element - عنصر پاسخ گلوکوکورتیکوئیدdominant negative - غالب منفی استPhosphate buffered saline - فسفات بافر شورFluticasone propionate - فلوتیکازون پروپیوناتRANTES - مطالبreverse transcriptase polymerase chain reaction - واکنش زنجیره ای پلی مراز ترانس کریتاز معکوسactivator protein 1 - پروتئین فعال کننده 1mitogen activated protein kinase - پروتئین کیناز فعال Mitogen فعال استchloramphenicol acetyltransferase - کلرامفنیکول استیل ترانسفرازextracellular regulated kinase - کیناز تنظیم شده خارج سلولی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی ریوی و تنفسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
IL-1β may contribute to airway inflammation by inducing pro-inflammatory cytokines and chemokines from bronchial epithelial cells. In the current study, we investigated the cis-acting sites within the IL-8 promoter, and signalling pathways important in IL-8 production from BEAS2B cells following IL-1β stimulation. IL-1β treatment (0.1-10 ng/mL) upregulated IL-8 protein production in a dose dependent manner and IL-8 mRNA in a time dependent manner. IL-1β induced upregulation of IL-8 promoter-reporter constructs, indicating that the mechanism of upregulation was pre-transcriptional. Using IL-8 promoter constructs with mutated cis-acting sites, it was found that both the NF-κB and NF-IL6 sites together were required for IL-8 promoter induction following IL-1β treatment. Using chemical inhibitors or dominant negative mutants, we found that IL-8 promoter activity required IκB kinase β, IκB, but not the MAP kinases p38 or c-Jun N-terminal kinase 2. Fluticasone propionate was able to suppress IL-1β induced IL-8 protein and promoter activation, using both a â1481 bp fragment and a â133 bp fragment, indicating that the glucocorticoid response element found at â330 bp was not required for fluticasone mediated suppression of IL-8 promoter activation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pulmonary Pharmacology & Therapeutics - Volume 18, Issue 5, October 2005, Pages 337-345
Journal: Pulmonary Pharmacology & Therapeutics - Volume 18, Issue 5, October 2005, Pages 337-345
نویسندگان
Michael R. Edwards, Naofumi Mukaida, Malcolm Johnson, Sebastian L. Johnston,