Role of cytokines in experimental colitis: relation to intestinal permeability.
Role of cytokines in experimental colitis: relation to intestinal permeability.
复制标题
细胞因子在实验性结肠炎中的作用：与肠道通透性的关系。
作者：
H. Tateishi;K. Mitsuyama;A. Toyonaga;M. Tomoyose;K. Tanikawa
现在有明确的证据支持细胞因子在人类炎症性肠病的临床和免疫病理表现中的作用。本研究的目的是确定细胞因子网络在三硝基苯磺酸诱导的大鼠结肠炎模型中的可能作用，并研究其与肠道通透性的关系。在伊文思蓝在结肠的肠道通透性迅速增加后，肿瘤坏死因子-α一过性增加，随后是白细胞介素1和白细胞介素6。免疫荧光染色显示肿瘤坏死因子-α和白介素1的产生细胞主要为巨噬细胞。反复注射白介素1受体拮抗剂导致髓过氧化物酶活性和结肠重量轻微下降。这些结果提示，肠巨噬细胞产生的促炎细胞因子增加，伴随着肠道通透性的增加，可能是导致三硝基苯磺酸诱导的结肠炎的肠道和全身特征的原因。药物阻断促炎细胞因子可能有助于减轻肠道炎症。
There is now clear evidence supporting the role of cytokines in the clinical and immunopathological manifestations of human inflammotory bowel disease. The purpose of the present study was to determine the possible role of a cytokine network in a rat model of trinitrobenzene sulfonic acid-induced colitis and to examine its relation to intestinal permeability. After a rapid increase in the intestinal permeability of Evans blue in the colon, tumor necrosis factor-alpha increased transiently, and interleukin-1 and interleukin-6 followed thereafter. The majority of tumor necrosis factor-alpha- and interleukin-1-producing cells observed by immunofluorescent staining was revealed to be macrophages. Repeated injections of interleukin-1 receptor antagonist led to a modest decrease in myeloperoxidase activity and colon weight. These findings suggest that enhanced pro-inflammatory cytokine production from intestinal macrophages accompanied by increased intestinal permeability may contribute to intestinal and systemic features of trinitrobenzene sulfonic acid-induced colitis. Pharmacologic blockade of pro-inflammatory cytokines may help reduce intestinal inflammation.