کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3296314 | 1209867 | 2007 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Gastroesophageal Reflux Disease-Associated Esophagitis Induces Endogenous Cytokine Production Leading to Motor Abnormalities
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کلمات کلیدی
TNFHEFGERDHEKPMA - LDC هاlactic acid dehydrogenase - اسید لاکتیک دهیدروژنازinterferon - اینترفرونIFN - اینترفرون هاinterleukin - اینترلوکینgastroesophageal reflux disease - بیماری ریفلاکس معده به مریELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاtumor necrosis factor - فاکتور نکروز تومورphorbol myristate acetate - فروبل مریستات استاتLDH - لاکتات دهیدروژناز به صورت مختصر شده LDH polymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمراز
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Gastroesophageal Reflux Disease-Associated Esophagitis Induces Endogenous Cytokine Production Leading to Motor Abnormalities Gastroesophageal Reflux Disease-Associated Esophagitis Induces Endogenous Cytokine Production Leading to Motor Abnormalities](/preview/png/3296314.png)
چکیده انگلیسی
Background & Aims: Gastroesophageal reflux disease is a condition frequently associated with esophagitis and motor abnormalities. Recent evidence suggests that proinflammatory cytokines, such as interleukin (IL)-1β and IL-6, may be implicated because they reduce esophageal muscle contractility, but these results derive from in vitro or animal models of esophagitis. This study used human esophageal cells and tissues to identify the cellular source of cytokines in human esophagitis investigate whether cytokines can be induced by gastric refluxate, and examine whether esophageal tissue- or cell-derived mediators affect muscle contractility. Methods: Endoscopic mucosal biopsy specimens were obtained from patients with and without esophagitis, organ-cultured, and undernatants were assessed for cytokine content. The cytokine profile of esophageal epithelial, fibroblast, and muscle cells was analyzed, and esophageal mucosa and cell products were tested in an esophageal circular muscle contraction assay. Results: The mucosa of esophagitis patients produced significantly greater amounts of IL-1β and IL-6 compared with those of control patients. Cultured esophageal epithelial cells produced IL-6, as did fibroblasts and muscle cells. Epithelial cells exposed to buffered, but not denatured, gastric juice produced IL-6. Undernatants of mucosal biopsy cultures from esophagitis patients reduced esophageal muscle contraction, as did supernatants from esophageal epithelial cell cultures. Conclusions: The human esophagus produces cytokines capable of reducing contractility of esophageal muscle cells. Exposure to gastric juice is sufficient to stimulate esophageal epithelial cells to produce IL-6, a cytokine able to alter esophageal contractility. These results indicate that classic cytokines are important mediators of the motor disturbances associated with human esophageal inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 132, Issue 1, January 2007, Pages 154-165
Journal: Gastroenterology - Volume 132, Issue 1, January 2007, Pages 154-165
نویسندگان
Florian Rieder, Ling Cheng, Karen M. Harnett, Amitabh Chak, Gregory S. Cooper, Gerard Isenberg, Monica Ray, Jeffry A. Katz, Andrew Catanzaro, Robert O'Shea, Anthony B. Post, Richard Wong, Michael V. Sivak, Thomas McCormick, Manijeh Phillips,