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肥大细胞及其主要分泌产物在炎症性肠病中的关键作用。

Key role of mast cells and their major secretory products in inflammatory bowel disease.

作者信息

He Shao-Heng

机构信息

Allergy and Inflammation Research Institute, Medical College, Shantou University, Shantou 515031, Guangdong Province, China.

出版信息

World J Gastroenterol. 2004 Feb 1;10(3):309-18. doi: 10.3748/wjg.v10.i3.309.

Abstract

Historically, mast cells were known as a key cell type involved in type I hypersensitivity. Until last two decades, this cell type was recognized to be widely involved in a number of non-allergic diseases including inflammatory bowel disease (IBD). Markedly increased numbers of mast cells were observed in the mucosa of the ileum and colon of patients with IBD, which was accompanied by great changes of the content in mast cells such as dramatically increased expression of TNFalpha, IL-16 and substance P. The evidence of mast cell degranulation was found in the wall of intestine from patients with IBD with immunohistochemistry technique. The highly elevated histamine and tryptase levels were detected in mucosa of patients with IBD, strongly suggesting that mast cell degranulation is involved in the pathogenesis of IBD. However, little is known of the actions of histamine, tryptase, chymase and carboxypeptidase in IBD. Over the last decade, heparin has been used to treat IBD in clinical practice. The low molecular weight heparin (LMWH) was effective as adjuvant therapy, and the patients showed good clinical and laboratory response with no serious adverse effects. The roles of PGD2, LTC4, PAF and mast cell cytokines in IBD were also discussed. Recently, a series of experiments with dispersed colon mast cells suggested there should be at least two pathways in man for mast cells to amplify their own activation-degranulation signals in an autocrine or paracrine manner. The hypothesis is that mast cell secretogogues induce mast cell degranulation, release histamine, then stimulate the adjacent mast cells or positively feedback to further stimulate its host mast cells through H1 receptor. Whereas released tryptase acts similarly to histamine, but activates mast cells through its receptor PAR-2. The connections between current anti-IBD therapies or potential therapies for IBD with mast cells were discussed, implicating further that mast cell is a key cell type that is involved in the pathogenesis of IBD. In conclusion, while pathogenesis of IBD remains unclear, the key role of mast cells in this group of diseases demonstrated in the current review implicates strongly that IBD is a mast cell associated disease. Therefore, close attentions should be paid to the role of mast cells in IBD.

摘要

从历史上看,肥大细胞被认为是参与I型超敏反应的关键细胞类型。直到过去二十年,人们才认识到这种细胞类型广泛参与包括炎症性肠病(IBD)在内的多种非过敏性疾病。在IBD患者的回肠和结肠黏膜中观察到肥大细胞数量显著增加,同时肥大细胞内的成分也发生了很大变化,如肿瘤坏死因子α、白细胞介素-16和P物质的表达显著增加。采用免疫组织化学技术在IBD患者的肠壁中发现了肥大细胞脱颗粒的证据。在IBD患者的黏膜中检测到组胺和类胰蛋白酶水平显著升高,强烈提示肥大细胞脱颗粒参与了IBD的发病机制。然而,关于组胺、类胰蛋白酶、糜蛋白酶和羧肽酶在IBD中的作用知之甚少。在过去十年中,肝素已被用于IBD的临床治疗。低分子量肝素(LMWH)作为辅助治疗有效,患者表现出良好的临床和实验室反应,且无严重不良反应。还讨论了前列腺素D2、白三烯C4、血小板活化因子和肥大细胞细胞因子在IBD中的作用。最近,一系列对分散的结肠肥大细胞进行的实验表明,在人类中,肥大细胞至少应有两条途径以自分泌或旁分泌方式放大其自身的激活-脱颗粒信号。假说是肥大细胞促分泌剂诱导肥大细胞脱颗粒,释放组胺,然后刺激相邻的肥大细胞或通过H1受体进行正反馈以进一步刺激其自身的肥大细胞。而释放的类胰蛋白酶作用与组胺相似,但通过其受体PAR-2激活肥大细胞。讨论了当前IBD的抗IBD治疗或潜在治疗与肥大细胞之间的联系,进一步表明肥大细胞是参与IBD发病机制的关键细胞类型。总之,虽然IBD的发病机制仍不清楚,但本综述中肥大细胞在这类疾病中的关键作用强烈提示IBD是一种与肥大细胞相关的疾病。因此,应密切关注肥大细胞在IBD中的作用。

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