Enhanced secretion of tumour necrosis factor-alpha, IL-6, and IL-1 beta by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn's disease.
Enhanced secretion of tumour necrosis factor-alpha, IL-6, and IL-1 beta by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn's disease.
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发表时间：
1993
影响因子：
4.6
通讯作者：
H. Reinecker;M. Steffen;T. Witthoeft;I. Pflueger;S. Schreiber;R. Macdermott;A. Raedler
中科院分区：
文献类型：
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作者：
H. Reinecker;M. Steffen;T. Witthoeft;I. Pflueger;S. Schreiber;R. Macdermott;A. Raedler
溃疡性结肠炎和克罗恩病中炎症的持续存在可能部分地通过促炎细胞因子的分泌增加来调节，所述促炎细胞因子的分泌增加是由于对初始刺激剂的适当响应和/或由于细胞因子分泌的下调受损。本研究的目的是确定促炎细胞因子肿瘤坏死因子-α（TNF-α），IL-6和IL-1 β的分泌模式，从分离的固有层单核细胞（LPMNC）从未经治疗的溃疡性结肠炎或克罗恩病患者的结肠活检分离。从炎症性肠病（IBD）粘膜中分离的LPMNC自发产生增加量的TNF-α、IL-6和IL-1 β。美洲商陆有丝分裂原刺激可进一步增强IBD LPMNC的TNF-α分泌。溃疡性结肠炎或克罗恩病患者LPMNC的TNF-α和IL-1 β分泌模式与组织受累程度和粘膜炎症密切相关。与未受累克罗恩病粘膜或对照粘膜相比，未受累溃疡性结肠炎粘膜的LPMNC分泌的IL-6水平显著升高。来自非受累溃疡性结肠炎粘膜的LPMNC的IL-6分泌增加，而没有可见的或显微镜下的炎症体征，表明溃疡性结肠炎和克罗恩病之间炎症起始中涉及的病理生理机制可能不同。通过从结肠镜活检中分离的LPMNC测定促炎细胞因子分泌可能是监测IBD患者粘膜炎症严重程度的敏感方法。
The perpetuation of inflammation in ulcerative colitis and Crohn's disease may be regulated in part by an increased secretion of proinflammatory cytokines due to either an appropriate response to initial stimulating agents, and/or due to an impaired down-regulation of cytokine secretion. The aim of this study was to determine the secretion patterns of the proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), IL-6 and IL-1 beta, from isolated lamina propria mononuclear cells (LPMNC) isolated from colonic biopsies from patients with untreated ulcerative colitis or Crohn's disease. LPMNC isolated from involved inflammatory bowel disease (IBD) mucosa spontaneously produced increased amounts of TNF-alpha, and IL-6, and IL-1 beta. The TNF-alpha secretion from IBD LPMNC could be further enhanced by pokeweed mitogen stimulation. The secretion patterns of TNF-alpha and IL-1 beta by LPMNC from patients with either ulcerative colitis or Crohn's disease demonstrated a close correlation with the degree of tissue involvement and mucosal inflammation. LPMNC from non-involved ulcerative colitis mucosa secreted markedly increased levels of IL-6 compared with non-involved Crohn's disease mucosa or control mucosa. The heightened IL-6 secretion from LPMNC from non-involved ulcerative colitis mucosa without visible or microscopic signs of inflammation indicates that the pathophysiologic mechanisms involved in the initiation of inflammation may differ between ulcerative colitis and Crohn's disease. The determination of proinflammatory cytokine secretion by isolated LPMNC from colonoscopic biopsies may be a sensitive method for monitoring the severity of mucosal inflammation in IBD patients.