کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8348336 | 1541724 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inflammation-induced functional connectivity of melanin-concentrating hormone and IL-10
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کلمات کلیدی
IBDMCHR1TNBSMCHIL-10DSS2,4,6-Trinitrobenzene sulfonic acid - 2،4،6-ترینیتروبنسل سولفونیک اسیدIntestinal inflammation - التهاب رودهInflammatory bowel disease - بیماریهای التهابی رودهGastrointestinal - دستگاه گوارشDextran sulfate sodium - سولفات سدیم دکسترانCytokines - سیتوکین هاMonocytes - مونوسیتهاNeuropeptides - نوروپپتیدهاmelanin-concentrating hormone - هورمون متمرکز کننده ملانینMelanin concentrating hormone - هورمون متمرکز کننده ملانینarbitrary units - واحد دلخواهAntibody - پادتَن یا آنتیبادی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Inflammation-induced functional connectivity of melanin-concentrating hormone and IL-10 Inflammation-induced functional connectivity of melanin-concentrating hormone and IL-10](/preview/png/8348336.png)
چکیده انگلیسی
Melanin-concentrating hormone (MCH) was identified in mammals as a hypothalamic neuropeptide regulating appetite and energy balance. However, similarly to most of the brain peptides, MCH is also produced in the gastrointestinal system and can act locally as an immunomodulator. We have previously reported high expression of MCH and its receptor MCHR1 in the affected mucosa of patients with inflammatory bowel disease. Furthermore, MCH deficiency in mice attenuated experimental colitis, pointing to MCH as a mediator of intestinal inflammation. In the present study, in order to gain further insights into the underlying mechanisms of such effects of MCH, we treated mice with established experimental colitis due to IL-10 deficiency with a MCHR1 antagonist (DABA-822). While treatment with the same drug was successful in attenuating TNBS-induced colitis in previous studies, it offered no benefit to the IL-10 knockout mouse model, suggesting that perhaps IL-10 is a downstream target of MCH. Indeed, in experiments focusing on monocytes, we found that treatment with MCH inhibited LPS-mediated IL-10 upregulation. Conversely, in the same cells, exogenous IL-10 prevented LPS-induced MCHR1 expression. Taken together, these findings indicate a functional cross-talk between MCH and IL-10 which prevents resolution of inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Peptides - Volume 55, May 2014, Pages 58-64
Journal: Peptides - Volume 55, May 2014, Pages 58-64
نویسندگان
Dimitrios C. Ziogas, Apostolos K.A. Karagiannis, Brenda M. Geiger, Beatriz Gras-Miralles, Robert Najarian, Ofer Reizes, Leo R. Fitzpatrick, Efi Kokkotou,