Hogan S P, Mishra A, Brandt E B, Royalty M P, Pope S M, Zimmermann N, Foster P S, Rothenberg M E
Division of Pulmonary Medicine, Allergy and Clinical Immunology, Department of Pediatrics, Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Nat Immunol. 2001 Apr;2(4):353-60. doi: 10.1038/86365.
Although eosinophils have been implicated in the pathogenesis of gastrointestinal disorders, their function has not been established. Using a murine model of oral antigen-induced eosinophil-associated gastrointestinal disease, we report the pathological consequences of eosinophilic inflammation and the involvement of eotaxin and eosinophils. Exposure of mice to enteric-coated antigen promotes an extensive T helper 2-associated eosinophilic inflammatory response involving the esophagus, stomach, small intestine and Peyer's patches as well as the development of gastric dysmotility, gastromegaly and cachexia. Electron microscopy shows eosinophils in proximity to damaged axons, which indicated that eosinophils were mediating a pathologic response. In addition, mice deficient in eotaxin have impaired eosinophil recruitment and are protected from gastromegaly and cachexia. These results establish a critical pathological function for eotaxin and eosinophils in gastrointestinal allergic hypersensitivity.
尽管嗜酸性粒细胞与胃肠道疾病的发病机制有关，但其功能尚未明确。利用口服抗原诱导的嗜酸性粒细胞相关胃肠道疾病的小鼠模型，我们报告了嗜酸性粒细胞炎症的病理后果以及嗜酸性粒细胞趋化因子和嗜酸性粒细胞的参与情况。给小鼠喂食肠溶抗原会引发广泛的与辅助性T细胞2相关的嗜酸性粒细胞炎症反应，累及食管、胃、小肠和派尔集合淋巴结，同时还会导致胃动力障碍、胃扩大和恶病质。电子显微镜显示嗜酸性粒细胞靠近受损轴突，这表明嗜酸性粒细胞正在介导一种病理反应。此外，缺乏嗜酸性粒细胞趋化因子的小鼠嗜酸性粒细胞募集受损，可免受胃扩大和恶病质的影响。这些结果确立了嗜酸性粒细胞趋化因子和嗜酸性粒细胞在胃肠道过敏性超敏反应中的关键病理功能。
