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世界核心医学期刊文摘（胃肠病学分册） 2006年第8期2卷 36-36页

作者： Lindsay j.O. Whelan K. stagg a.j. 程妍 Barts and the London NHS Trust Royal London Hospital London E1 1BB United Kingdom Dr.

Background and aims: The intestinal microbiota play a pivotal role in the inflammation associated with Crohn’s disease through their interaction with the mucosal immune system. Some bifidobacteria species are immunoregulatory and induce increased dendritic cell interleukin 10 (IL- 10) release in vitro. Fructo-oligosaccharides (FOS) increase faecal and mucosal bifidobacteria in healthy volunteers. The aim of this study was to assess the effect of FOS administration on disease activity, bifidobacteria concentrations, and mucosal dendritic cell function in patients with moderately active Crohn’s disease. Patients and methods: Ten patients with active ileocolonic Crohn’s disease received 15 g of FOS for three weeks. Disease activity was measured using the Harvey Bradshaw index. Faecal and mucosal bifidobacteria were quantified by fluorescence in situ hybridisation, and mucosal dendritic cell IL- 10 and Toll-like receptor (TLR) expression were assessed by flow cytometry of dissociated rectal biopsies. Results: FOS induced a significant reduction in the Harvey Bradshaw index from 9.8 (SD 3.1) to 0.9 (3.4) (p < 0.01). There was a significant increase in faecal bifidobacteria concentration from 8.8 (0.9) log10 to 9.4 (0.9)- log10 cells/g dry faeces (p < 0.001). The percentage of IL- 10 positive dendritic cells increased from 30 (12)% to 53 (10)% (p = 0.06). Finally, the percentage of dendritic cells expressing TLR2 and TLR4 increased from 1.7 (1.7)% to 36.8 (15.9)% (p = 0.08) and from 3.6 (3.6)% to 75.4 (3.4)% (p < 0.001), respectively. Conclusions: FOS supplementation increases faecal bifidobacteria concentrations and modifies mucosal dendritic cell function. This novel therapeutic strategy appears to decrease Crohn’s disease activity in a small open label trial and therefore warrants further investigation.

关键词：结肠克罗恩病低聚果糖免疫学效果患者微生物学黏膜免疫系统树突状细胞 Toll样受体流式细胞仪分析疾病活动度

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炎症性肠病患者肠道树突状细胞的特性

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世界核心医学期刊文摘（胃肠病学分册） 2005年第12期1卷 25-26页

作者： Hart A.L. Al- Hassi H.O. Rigby R.j. a.j. stagg 王志宇 Antigen Presentation Research Gro- up Imperial College London Northwick Park Campus Watford Road Harrow HA1 3UJ United Kingdom Dr.

Background & Aims: Dendritic cells (DCs) recognize and respond to microbial structures using pattern recognition receptors, including Toll- like receptors (TLRs). In the intestine, DCs are pivotal in tolerance induction and direct the differentiation of T cells. We aimed to identify changes in intestinal DCs that may underlie the dysregulated immune response to enteric bacteria that occurs in patients with inflammatory bowel disease (IBD). Methods: DCs were identified in freshly isolated lamina propria mononuclear cells by multicolor flow cytometry in patients with IBD and controls. Expression of TLR2, TLR4, and the activation/mat- uration marker CD40 was assessed by cell surface labeling. Production of cytokines (interleukin [IL]- 12, IL- 6, and IL- 10) was assessed in the absence of exogenous stimulation by intracellular staining of permeabilized cells. Results: In healthy controls, few intestinal DCs expressed TLR2 or TLR4, in contrast to blood DCs. DC expression of both TLRs was significantly enhanced in Crohn’ s disease and ulcerative colitis. DCs from inflamed tissue of patients with Crohn’ s disease expressed significantly higher levels of the maturation/activation marker CD40. Elevated levels of CD40 on DCs were decreased after treating patients with anti- tumor necrosis factor α . In Crohn’ s disease, but not ulcerative colitis, more colonic DCs produced IL- 12 and IL- 6. The number of IL- 10- producing DCs did not differ significantly between patients with IBD and controls. Conclusions: In IBD, DCs are activated, their expression of microbial recognition receptors is up- regulated, and more DCs produce pathologically relevant cytokines. Intestinal DCs are likely to be key initiators or perpetuators of the inflammatory response that characterizes IBD.

关键词：炎症性肠病树突状细胞克罗恩病黏膜固有层非溃疡性结肠炎多色流式细胞细胞表面标志细胞因子胞外刺激细胞分化

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