Straumann A, Bauer M, Fischer B, Blaser K, Simon H U
Department of Gastroenterology, Kantonsspital, Olten, Switzerland.
J Allergy Clin Immunol. 2001 Dec;108(6):954-61. doi: 10.1067/mai.2001.119917.
Idiopathic eosinophilic esophagitis (IEE) is a chronic-inflammatory disorder of the esophagus of unknown origin. The established cornerstone of diagnosis is a dense infiltration of the esophagus with eosinophils, but neither the precise pattern of inflammatory cell infiltration nor the mechanisms that likely contribute to induction and maintenance of the inflammatory response have been described.
The intention of this study was to characterize the esophageal inflammatory infiltrate and the expression of cytokines in the esophagus in this disease. In addition, we searched for immunologic abnormalities of blood leukocytes to exclude major primary hyporeactive and hyperreactive conditions of the immune system.
Infiltration of inflammatory cells in the esophagus, stomach, and duodenum was analyzed by immunohistochemistry through use of mAbs against lineage-associated molecules. Cytokine expression was measured by ELISA and immunohistochemical analysis. Lymphocyte subpopulations in blood were determined by means of flow cytometry.
High eosinophil infiltration into the esophageal squamous epithelium was observed in patients with IEE but not in control subjects. Interestingly, increased T-cell and mast cell numbers were also found within the epithelium in these patients. In contrast, the numbers of inflammatory cells were not increased in the stomach and duodenum in patients with IEE, suggesting a specific inflammatory process within the esophagus. Moreover, increased expression of IL-5 and TNF-alpha was observed in esophageal epithelial biopsy specimens. The distribution of lymphocyte subsets in the peripheral blood and their capacity to generate cytokines did not reflect the changes observed at the inflammatory site.
IEE is a selective inflammatory response of the esophagus. T cells, IL-5, eosinophils, and IgE-mediated mechanisms appear to be involved, giving rise to the possibility that allergic reactions might play a role in the pathogenesis of the disease.
特发性嗜酸性粒细胞性食管炎（IEE）是一种病因不明的食管慢性炎症性疾病。已确立的诊断基石是食管中嗜酸性粒细胞的密集浸润，但炎症细胞浸润的确切模式以及可能导致炎症反应诱导和维持的机制尚未得到描述。
本研究旨在描述该疾病中食管的炎症浸润情况以及食管中细胞因子的表达。此外，我们寻找血液白细胞的免疫异常情况，以排除免疫系统主要的原发性低反应性和高反应性疾病。
通过使用针对谱系相关分子的单克隆抗体，采用免疫组织化学方法分析食管、胃和十二指肠中的炎症细胞浸润情况。通过酶联免疫吸附测定（ELISA）和免疫组织化学分析测量细胞因子表达。采用流式细胞术测定血液中的淋巴细胞亚群。
在IEE患者中观察到食管鳞状上皮中有高嗜酸性粒细胞浸润，而在对照受试者中未观察到。有趣的是，在这些患者的上皮内还发现T细胞和肥大细胞数量增加。相比之下，IEE患者的胃和十二指肠中的炎症细胞数量没有增加，提示食管内存在特定的炎症过程。此外，在食管上皮活检标本中观察到白细胞介素-5（IL-5）和肿瘤坏死因子-α（TNF-α）表达增加。外周血中淋巴细胞亚群的分布及其产生细胞因子的能力并未反映在炎症部位观察到的变化。
IEE是食管的一种选择性炎症反应。T细胞、IL-5、嗜酸性粒细胞和IgE介导的机制似乎参与其中，这使得过敏反应可能在该疾病的发病机制中起作用。
