Paul Gisela, Schäffler Andreas, Neumeier Markus, Fürst Alois, Bataillle Frauke, Buechler Christa, Müller-Ladner Ulf, Schölmerich Jürgen, Rogler Gerhard, Herfarth Hans
Department of Internal Medicine I, University of Regensburg, Regensburg, Germany.
Inflamm Bowel Dis. 2006 Jun;12(6):471-7. doi: 10.1097/00054725-200606000-00005.
Adipose tissue is recognized as a compartment secreting highly active molecules. Creeping fat represents a characteristic feature of Crohn's disease (CD). Proinflammatory or anti-inflammatory adipose-derived secretory products, now generally called adipocytokines, may play a role in the pathogenesis of CD.
Adipose tissue specimens were obtained from creeping fat contiguous to the involved intestine of 10 patients with CD. Mesenteric adipose tissue specimens resected from 13 patients with colon cancer (CC) and from 7 patients with diverticulitis served as controls. Three fat tissue specimen per well and 6 to 8 wells per patient were incubated ex vivo for 24 h. The release of adiponectin, resistin, leptin, interleukin-6, macrophage colony-stimulating factor, monocyte chemotactic protein-1, and migration inhibitory factor was measured by ELISA. The expression of AdipoR1 and AdipoR2 receptors was investigated by real-time quantitative polymerase chain reaction in a subset of adipose tissues.
The secretion of adiponectin and macrophage colony-stimulating factor, as well as leptin and migration inhibitory factor, was significantly upregulated in CD compared with CC and diverticulitis or CC only, respectively. Resistin, interleukin-6, and monocyte chemotactic protein-1 were not specifically induced in CD but were associated with unspecific inflammation. Adiponectin receptor expression was not different in CC, CD, or diverticulitis. Steroid treatment in CD patients had differential effects on the ex vivo secretion of adipocytokines.
A specific secretion pattern of proinflammatory and anti-inflammatory adipocytokines indicates the significance of adipose tissue in intestinal inflammation in CD. Future investigations of this intestinal compartment may provide novel insights into the pathophysiological role of creeping fat and CD.
脂肪组织被认为是一个分泌高活性分子的隔室。匐行脂肪是克罗恩病（CD）的一个特征性表现。促炎或抗炎性脂肪源性分泌产物，现通常称为脂肪细胞因子，可能在CD的发病机制中起作用。
从10例CD患者受累肠段相邻的匐行脂肪中获取脂肪组织标本。从13例结肠癌（CC）患者和7例憩室炎患者切除的肠系膜脂肪组织标本作为对照。每孔接种3个脂肪组织标本，每位患者6至8孔，进行体外培养24小时。采用酶联免疫吸附测定法（ELISA）检测脂联素、抵抗素、瘦素、白细胞介素-6、巨噬细胞集落刺激因子、单核细胞趋化蛋白-1和迁移抑制因子的释放。通过实时定量聚合酶链反应在一部分脂肪组织中研究脂联素受体1（AdipoR1）和脂联素受体2（AdipoR2）的表达。
与CC组和憩室炎组或仅CC组相比，CD组脂联素和巨噬细胞集落刺激因子以及瘦素和迁移抑制因子的分泌分别显著上调。抵抗素、白细胞介素-6和单核细胞趋化蛋白-1在CD中并非特异性诱导产生，而是与非特异性炎症相关。CC组、CD组或憩室炎组中脂联素受体的表达无差异。CD患者的类固醇治疗对脂肪细胞因子的体外分泌有不同影响。
促炎和抗炎脂肪细胞因子的特定分泌模式表明脂肪组织在CD肠道炎症中的重要性。对这个肠道隔室的进一步研究可能为匐行脂肪和CD的病理生理作用提供新的见解。
