کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3296380 | 1209868 | 2008 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hypoxia-Independent Activation of HIF-1 by Enterobacteriaceae and Their Siderophores
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کلمات کلیدی
SalmochelinHMECsDFOiutAAerobactinACTADMPO2HIFAEBDesferrioxaminePHDMOI - MESAL - WILLActinomycin - آتیینومایسینadrenomedullin - آدرنومدولینIron - آهنVascular endothelial growth factor - فاکتور رشد اندوتلیال عروقیVascular Endothelial Growth Factor (VEGF) - فاکتور رشد اندوتلیال عروقی (VEGF)Hypoxia Inducible Factor - فاکتور قابل تشخیص هیپوکسیhexokinase - هگزوکینازPeyer’s patches - پیک هاmultiplicity of infection - چندین عفونت
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: Hypoxia inducible factor-1 (HIF-1) is the key transcriptional regulator during adaptation to hypoxia. Recent studies provide evidence for HIF-1 activation during bacterial infections. However, molecular details of how bacteria activate HIF-1 remain unclear. Here, we pursued the role of bacterial siderophores in HIF-1 activation during infection with Enterobacteriaceae. Methods: In vivo, HIF-1 activation and HIF-1-dependent gene induction in Peyer's patches were analyzed after orogastric infection with Yersinia enterocolitica. The course of an orogastric Y enterocolitica infection was determined using mice with a deletion of HIF-1α in the intestine. In vitro, the mechanism of HIF-1 activation was analyzed in infections with Y enterocolitica, Salmonella enterica subsp enterica, and Enterobacter aerogenes. Results: Infection of mice with Y enterocolitica led to functional activation of HIF-1 in Peyer's patches. Because mice with deletion of HIF-1α in the intestinal epithelium showed a significantly higher susceptibility to orogastric Y enterocolitica infections, bacterial HIF-1 activation appears to represent a host defense mechanism. Additional studies with Y enterocolitica, S enterica subsp enterica, or E aerogenes, and, moreover, application of their siderophores (yersiniabactin, salmochelin, aerobactin) caused a robust, dose-dependent HIF-1 response in human epithelia and endothelia, independent of cellular hypoxia. HIF-1 activation occurs most likely because of inhibition of prolylhydroxylase activity and is abolished upon infection with siderophore uptake deficient bacteria. Conclusions: Taken together, this study reveals what we believe to be a previously unrecognized role of bacterial siderophores for hypoxia-independent activation of HIF-1 during infection with human pathogenic bacteria.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 134, Issue 3, March 2008, Pages 756-767.e6
Journal: Gastroenterology - Volume 134, Issue 3, March 2008, Pages 756-767.e6
نویسندگان
Hanna Hartmann, Holger K. Eltzschig, Helena Wurz, Klaus Hantke, Alexander Rakin, Amir S. Yazdi, Gianluca Matteoli, Erwin Bohn, Ingo B. Autenrieth, Jörn Karhausen, Diana Neumann, Sean P. Colgan, Volkhard A.J. Kempf,