Mesenteric fat as a source of C reactive protein and as a target for bacterial translocation in Crohn's disease.
Mesenteric fat as a source of C reactive protein and as a target for bacterial translocation in Crohn's disease.
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DOI：
10.1136/gutjnl-2011-300370
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发表时间：
2012-01
期刊：
影响因子：
24.5
通讯作者：
Desreumaux P
中科院分区：
文献类型：
--
作者：
Peyrin-Biroulet L;Gonzalez F;Dubuquoy L;Rousseaux C;Dubuquoy C;Decourcelle C;Saudemont A;Tachon M;Béclin E;Odou MF;Neut C;Colombel JF;Desreumaux P
肠系膜脂肪增生是克罗恩病（CD）的标志，C反应蛋白（CRP）与疾病活动性相关。作者研究了肠系膜脂肪细胞是否可能是CD中CRP的来源，以及炎症和细菌触发因素是否可能刺激脂肪细胞产生CRP。评估CD患者肠系膜和皮下脂肪中CRP的表达以及CRP血浆浓度与肠系膜信使RNA （mRNA）水平的相关性。使用脂肪细胞系测试炎症和细菌挑战对CRP合成的影响。在结肠炎、回肠炎实验模型和CD患者中研究了细菌向肠系膜脂肪的易位。CD患者肠系膜脂肪中CRP表达升高，mRNA水平分别是溃疡性结肠炎患者肠系膜脂肪和同一CD患者皮下脂肪的80±40倍（p<0.05）和140±65倍（p=0.04），并与血浆水平相关。大肠杆菌（1230±175倍，p<0.01）、脂多糖（26±0.5倍，p<0.01）、肿瘤坏死因子α（15±0.3倍，p<0.01）、白细胞介素-6（10±0.7倍，p<0.05）升高脂肪细胞3T3-L1 CRP mRNA水平。细菌易位到肠系膜脂肪的发生率分别为13%和27%的健康和乳糜泻受试者，并且在实验性结肠炎和回肠炎中增加。人肠系膜脂肪细胞组成性表达TLR2、TLR4、NOD1和NOD2的mRNA。肠系膜脂肪是CD中CRP的重要来源。肠系膜脂肪细胞产生CRP可能由局部炎症和细菌易位到肠系膜脂肪触发，这提供了一种机制，即肠系膜脂肪增生可能有助于CD的炎症反应。
Mesenteric fat hyperplasia is a hallmark of Crohn's disease (CD), and C reactive protein (CRP) is correlated with disease activity. The authors investigated whether mesenteric adipocytes may be a source of CRP in CD and whether inflammatory and bacterial triggers may stimulate its production by adipocytes. CRP expression in the mesenteric and subcutaneous fats of patients with CD and the correlation between CRP plasma concentrations and mesenteric messenger RNA (mRNA) levels were assessed. The impact of inflammatory and bacterial challenges on CRP synthesis was tested using an adipocyte cell line. Bacterial translocation to mesenteric fat was studied in experimental models of colitis and ileitis and in patients with CD. CRP expression was increased in the mesenteric fat of patients with CD, with mRNA levels being 80±40 (p<0.05) and 140±65 (p=0.04) times higher than in the mesenteric fat of patients with ulcerative colitis and in the subcutaneous fat of the same CD subjects, respectively, and correlated with plasma levels. Escherichia coli (1230±175-fold, p<0.01), lipopolysaccharide (26±0.5-fold, p<0.01), tumour necrosis factor α (15±0.3-fold, p<0.01) and interleukin-6 (10±0.7-fold, p<0.05) increased CRP mRNA levels in adipocyte 3T3-L1 cells. Bacterial translocation to mesenteric fat occurred in 13% and 27% of healthy and CD subjects, respectively, and was increased in experimental colitis and ileitis. Human mesenteric adipocytes constitutively expressed mRNA for TLR2, TLR4, NOD1 and NOD2. Mesenteric fat is an important source of CRP in CD. CRP production by mesenteric adipocytes may be triggered by local inflammation and bacterial translocation to mesenteric fat, providing a mechanism whereby mesenteric fat hyperplasia may contribute to inflammatory response in CD.
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