کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8749323 1593668 2018 22 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Fecal bacteria from Crohn's disease patients more potently activated NOD-like receptors and Toll-like receptors in macrophages, in an IL-4-repressible fashion
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی میکروب شناسی
پیش نمایش صفحه اول مقاله
Fecal bacteria from Crohn's disease patients more potently activated NOD-like receptors and Toll-like receptors in macrophages, in an IL-4-repressible fashion
چکیده انگلیسی
Crohn's disease (CD) is characterized by a pathogenic intestinal inflammation mediated by a Th1-skewed immune system and a dysregulated intestinal mucosal community. In this study, we investigated the role of bacteria on the activation and function of monocytes, and its association with CD pathogenesis. To this end, fecal bacteria from CD patients and healthy controls were collected and used to stimulate autologous circulating monocytes. Fecal bacteria from CD patients were more effective at upregulating NOD2, NLRP3, TLR2, and TLR4 expression than fecal bacteria from healthy controls. Furthermore, the monocyte-derived macrophages (MDMs) induced by CD bacteria were more sensitive to E. coli stimulation than the MDMs induced by control bacteria, and demonstrated more M1 characteristics with high IL-6, TNF-α, and IL-12 and low IL-4 production. These effects mediated by fecal bacteria from CD patients could be repressed by the supplementation of IL-4. IL-4 not only suppressed the expression of NOD1, NOD2, NLRP3, TLR2, TLR4, and CD14 in MDMs induced by CD bacteria, but also suppressed E. coli-mediated expression of IL-6, TNF-α, and IL-12. Furthermore, IL-4-conditioned MDMs were more effective at supporting Th2 differentiation and inhibiting Th1 and Th17 differentiation of CD4+ T cells. Together, these studies demonstrated that fecal bacteria from CD patients presented enhanced capacity to upregulate pattern-recognition molecules in macrophages, which could be repressed by IL-4.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbial Pathogenesis - Volume 121, August 2018, Pages 40-44
نویسندگان
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