Veres G, Helin T, Arato A, Färkkilä M, Kantele A, Suomalainen H, Savilahti E
Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland.
Clin Immunol. 2001 Jun;99(3):353-9. doi: 10.1006/clim.2001.5032.
The mechanisms of adverse reactions to foods in the gastrointestinal tract are poorly understood. Previous studies of other atopic diseases and animal models suggest that adhesion molecules and mucosal lymphocytes may be implicated in the pathogenesis of food allergy (FA). The aim of our study was to investigate the expression of adhesion molecules and mucosal lymphocytes in duodena of patients with food allergies and of controls. Ten patients with FA to cereals (wheat, oats, and rye) or cow's milk and 9 control patients were included in the study. Quantitative analysis and immunohistochemical stainings for two pairs of adhesion molecules (intercellular adhesion molecule-1 (ICAM-1), lymphocyte function-associated antigen-1 (LFA-1), alpha4beta7 integrin, and mucosal addressin cell adhesion molecule (MAdCAM-1) and lymphocyte markers on endoscopic duodenal biopsy specimens were performed. The villous structure and density of LFA-1-positive cells were normal in every biopsy specimen, but the patients had significantly more alpha4beta7+ cells in the intraepithelial space (P = 0.01). The expression of ICAM-1 in the lamina propria of patients with FA was also substantially increased (P = 0.003); however, staining with MAdCAM showed no intergroup difference. Moreover, we found significantly increased CD4+ and HLA-DR+ cells in the lamina propria of patients, in comparison to the controls, P = 0.05 and P = 0.04, respectively. The densities of CD3, CD8, HLA-DP, T cell receptor alphabeta+ and gammadelta+ cells and IgA-, IgA1-, and IgA2-containing cells did not differ in the two groups studied. Our results suggest that the increased expression of ICAM-1 and alpha4beta7 integrin may play an important role in the pathogenesis of food hypersensitivity and with the elevation of CD4- and HLA-DR-positive cells reflect a stage of inflammation in the structurally normal intestines.
胃肠道对食物不良反应的机制尚不清楚。以往对其他特应性疾病和动物模型的研究表明,黏附分子和黏膜淋巴细胞可能与食物过敏(FA)的发病机制有关。我们研究的目的是调查食物过敏患者和对照组十二指肠中黏附分子和黏膜淋巴细胞的表达情况。本研究纳入了10名对谷物(小麦、燕麦和黑麦)或牛奶过敏的患者以及9名对照患者。对内镜下十二指肠活检标本进行了两对黏附分子(细胞间黏附分子-1(ICAM-1)、淋巴细胞功能相关抗原-1(LFA-1)、α4β7整合素和黏膜地址素细胞黏附分子(MAdCAM-1))以及淋巴细胞标志物的定量分析和免疫组化染色。每个活检标本中LFA-1阳性细胞的绒毛结构和密度均正常,但患者上皮内空间中的α4β7+细胞明显更多(P = 0.01)。FA患者固有层中ICAM-1的表达也显著增加(P = 0.003);然而,MAdCAM染色显示组间无差异。此外,与对照组相比,我们发现患者固有层中的CD4+和HLA-DR+细胞显著增加,P值分别为0.05和0.04。在所研究的两组中,CD3、CD8、HLA-DP、T细胞受体αβ+和γδ+细胞以及含IgA、IgA1和IgA2的细胞的密度没有差异。我们的结果表明,ICAM-1和α4β7整合素表达的增加可能在食物超敏反应的发病机制中起重要作用,并且随着CD4和HLA-DR阳性细胞的增加反映了结构正常的肠道中的炎症阶段。
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