کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10814902 | 1058433 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Activation of TOLLIP by porin prevents TLR2-associated IFN-γ and TNF-α-induced apoptosis of intestinal epithelial cells
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کلمات کلیدی
SLSEthD-1PRRIBDOMPTLRPFAethidium homodimer-1 - اتودیم homodimer-1Microbe-associated molecular pattern - الگوی مولکولی مرتبط با میکروبinterferon-γ - اینترفرون-γInflammatory bowel disease - بیماریهای التهابی رودهanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancetumor necrosis factor-α - تومور نکروز عامل αToll-like receptor - تیالآرTollip - سفارشیintestinal epithelial cell - سلول های اپیتلیال رودهIntestinal epithelial cells - سلولهای اپیتلیال رودهphycoerythrin - فایکوئیریدینMAMP - مامانAntibody - پادتَن یا آنتیبادیparaformaldehyde - پارافرمالدهیدtoll-interacting protein - پروتئین تلفنی متقابلOuter membrane protein - پروتئین غشای خارجیPropidium iodide - پروتئین یدیدPorin - پوریIEC - کمیسیون مستقل انتخاباتToll-like receptor 2 - گیرنده تله مانند 2pattern recognition receptor - گیرنده شناسایی الگو
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Activation of TOLLIP by porin prevents TLR2-associated IFN-γ and TNF-α-induced apoptosis of intestinal epithelial cells Activation of TOLLIP by porin prevents TLR2-associated IFN-γ and TNF-α-induced apoptosis of intestinal epithelial cells](/preview/png/10814902.png)
چکیده انگلیسی
Interferon (IFN)-γ and tumor necrosis factor (TNF)-α cause chronic inflammation of the intestine leading to progression of inflammatory bowel disease (IBD), which is manifested through rapid apoptosis of the intestinal epithelial cells (iECs). Here, we show inhibition of IFN-γ and TNF-α-induced apoptosis of INT-407 cells by porin, a microbe-associated molecular pattern (MAMP) with affinity for toll-like receptor (TLR)2 and commonly present in Gram-negative bacteria. Proinflammatory cytokines induce apoptosis by activation of caspase 8 that triggers caspase 9 through Bax finally leading to activation of caspase 3, the executioner caspase. Interestingly, while IFN-γ and TNF-α promotes Bax expression, in contrast porin up-regulates anti-apoptotic Bcl-xL resulting in iEC survivability. We show elevated expression of TLR2 is a key requisite for IFN-γ and TNF-α mediated caspase 8 up-regulation that contributes to apoptosis of iECs. Down-regulation of TLR2 expression is central for checking apoptosis which is achieved by elevated level of toll-interacting protein (TOLLIP) in presence of porin. Attempts to limit IBD is in progress with anti-IFN-γ and anti-TNF-α Abs or use of IL-10. Although probiotic bacterial proteins have shown to successfully reduce IFN-γ and TNF-α mediated apoptosis, the exact mechanism of their action has remained elusive. This study identifies the underlying sequential events of transient TLR2 stimulation followed by its blocking in response to the bacterial outer membrane protein, which advocates intervention at TLR-juncture is crucial for controlling IBD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 26, Issue 12, December 2014, Pages 2674-2682
Journal: Cellular Signalling - Volume 26, Issue 12, December 2014, Pages 2674-2682
نویسندگان
Subhadeep Mukherjee, Tapas Biswas,