Effects of obesity on severity of colitis and cytokine expression in mouse mesenteric fat. Potential role of adiponectin receptor 1.
Effects of obesity on severity of colitis and cytokine expression in mouse mesenteric fat. Potential role of adiponectin receptor 1.
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肥胖对结肠炎严重程度和小鼠肠系膜脂肪细胞因子表达的影响。
DOI：
10.1152/ajpgi.00269.2014
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Karagiannides,Iordanes
中科院分区：
文献类型：
--
作者：
Sideri,Aristea;Stavrakis,Dimitris;Bowe,Collin;Shih,DavidQ;Fleshner,Phillip;Arsenescu,Violeta;Arsenescu,Razvan;Turner,JerroldR;Pothoulakis,Charalabos;Karagiannides,Iordanes
在炎症性肠病（IBD）中，肥胖与疾病过程的恶化有关。在这里，我们研究了肥胖在结肠炎发展中的作用，并研究了IBD患者肠系膜脂肪上皮细胞的相互作用。我们将饮食诱导的肥胖与三硝基苯磺酸（TNBS）结肠炎小鼠模型相结合，以创建肥胖、结肠炎及其组合的组。肠系膜脂肪和肠的变化进行了评估，组织学，髓过氧化物酶测定，细胞因子mRNA表达的实时PCR。从肥胖患者和IBD患者中获得来自人肠系膜脂肪和培养的前脂肪细胞的培养基。组织学分析显示，与所有其他组相比，患有结肠炎的肥胖小鼠的肠道和肠系膜脂肪中炎症细胞浸润和组织损伤增加。肥胖还增加了促炎细胞因子的表达，包括IL-1β、TNF-α、单核细胞趋化蛋白1和角质形成细胞衍生的趋化因子，同时减少了TNBS诱导的肠系膜脂肪和肠组织中IL-2和IFN-γ的增加。与对照组相比，从肥胖患者和IBD患者中分离的人肠系膜脂肪表现出脂肪因子和生长因子的差异释放。脂肪条件培养基降低人NCM 460结肠上皮细胞中脂联素受体1（AdipoR 1）的表达。小鼠结肠内AdipoR 1沉默加重TNBS诱导的结肠炎总之，肥胖是实验性结肠炎的结果，肥胖和IBD相关的脂肪组织变化促进肠系膜脂肪中调节结肠细胞反应的差异介质释放，并可能影响结肠炎的病程。我们的研究结果还表明，AdipoR 1在结肠炎期间的炎症调节中对脂肪-肠轴起着重要作用。
In inflammatory bowel disease (IBD), obesity is associated with worsening of the course of disease. Here, we examined the role of obesity in the development of colitis and studied mesenteric fat-epithelial cell interactions in patients with IBD. We combined the diet-induce obesity with the trinitrobenzene sulfonic acid (TNBS) colitis mouse model to create groups with obesity, colitis, and their combination. Changes in the mesenteric fat and intestine were assessed by histology, myeloperoxidase assay, and cytokine mRNA expression by real-time PCR. Medium from human mesenteric fat and cultured preadipocytes was obtained from obese patients and those with IBD. Histological analysis showed inflammatory cell infiltrate and increased histological damage in the intestine and mesenteric fat of obese mice with colitis compared with all other groups. Obesity also increased the expression of proinflammatory cytokines including IL-1β, TNF-α, monocyte chemoattractant protein 1, and keratinocyte-derived chemokine, while it decreased the TNBS-induced increases in IL-2 and IFN-γ in mesenteric adipose and intestinal tissues. Human mesenteric fat isolated from obese patients and those with and IBD demonstrated differential release of adipokines and growth factors compared with controls. Fat-conditioned media reduced adiponectin receptor 1 (AdipoR1) expression in human NCM460 colonic epithelial cells. AdipoR1 intracolonic silencing in mice exacerbated TNBS-induced colitis. In conclusion, obesity worsens the outcome of experimental colitis, and obesity- and IBD-associated changes in adipose tissue promote differential mediator release in mesenteric fat that modulates colonocyte responses and may affect the course of colitis. Our results also suggest an important role for AdipoR1 for the fat-intestinal axis in the regulation of inflammation during colitis.
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DOI：
10.1530/joe-13-0339
发表时间：
2014-02
期刊：
The Journal of endocrinology
影响因子：
--
作者：
Cao H
通讯作者：
Cao H
影响因子：
29.4
作者：
Fayad, Raja;Pini, Maria;Fantuzzi, Giamila
通讯作者：
Fantuzzi, Giamila
DOI：
10.1152/ajpregu.2001.280.6.r1772
发表时间：
2001-06-01
影响因子：
2.8
作者：
Karagiannides, I;Tchkonia, T;Kirkland, JL
通讯作者：
Kirkland, JL
DOI：
10.1073/pnas.0600821103
发表时间：
2006-03-28
影响因子：
11.1
作者：
Karagiannides, L;Kokkotou, E;Pothoulakis, C
通讯作者：
Pothoulakis, C
影响因子：
9.8
作者：
Chan, Simon S. M.;Luben, Robert;Hart, Andrew R.
通讯作者：
Hart, Andrew R.