Levy A M, Yamazaki K, Van Keulen V P, Burgart L J, Sandborn W J, Phillips S F, Kephart G M, Gleich G J, Leiferman K M
Department of Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
Am J Gastroenterol. 2001 May;96(5):1522-8. doi: 10.1111/j.1572-0241.2001.03750.x.
Eosinophils infiltrate the colonic mucosa of patients with collagenous colitis (CC), although the pathogenetic implications are unknown, including whether these eosinophils are activated and degranulate in situ. We examined eosinophil infiltration and degranulation in the intestines of patients with CC by immunofluorescence for eosinophil granule major basic protein (MBP).
We used both conventional histology (hematoxylin and eosin) and indirect MBP immunofluorescence histochemistry on colon biopsy specimens from patients with CC (n = 21) and from healthy controls (n = 9). Scoring of histological features was performed on hematoxylin and eosin-stained sections on a 0 to 3 scale. Eosinophil infiltration and degranulation, as quantified by extracellular MBP staining, were scored in each specimen on a 0 to 4 scale.
The inflammatory infiltrate of the lamina propria, the thickness of the collagen band, the numbers of intraepithelial lymphocytes, and degree of epithelial cell damage were all significantly increased in patients with CC as compared to controls (p < 0.0001). Scores for both eosinophil infiltration and degranulation were also significantly higher in the CC group compared to controls (p < 0.0001). The degree of infiltrating eosinophils by hematoxylin and eosin was correlated with eosinophil infiltration and degranulation by MBP immunostaining; however, no other correlations were found between eosinophil infiltration or degranulation by immunofluorescence and any of the histological parameters measured in the CC group.
Eosinophil infiltration and degranulation are increased in the colonic mucosa of patients with CC compared to healthy controls. Eosinophils and their cytotoxic granule proteins could be involved in the pathogenesis of CC. Further studies will be necessary to elucidate the mechanisms of eosinophil activation in CC.
嗜酸性粒细胞浸润胶原性结肠炎（CC）患者的结肠黏膜，但其致病意义尚不清楚，包括这些嗜酸性粒细胞是否在原位被激活并脱颗粒。我们通过对嗜酸性粒细胞颗粒主要碱性蛋白（MBP）进行免疫荧光检测，研究了CC患者肠道中的嗜酸性粒细胞浸润和脱颗粒情况。
我们对21例CC患者和9例健康对照者的结肠活检标本同时采用传统组织学方法（苏木精和伊红染色）和间接MBP免疫荧光组织化学方法。在苏木精和伊红染色切片上对组织学特征进行0至3分的评分。通过细胞外MBP染色定量的嗜酸性粒细胞浸润和脱颗粒情况，在每个标本上进行0至4分的评分。
与对照组相比，CC患者固有层的炎性浸润、胶原带厚度、上皮内淋巴细胞数量及上皮细胞损伤程度均显著增加（p<0.0001）。CC组的嗜酸性粒细胞浸润和脱颗粒评分也显著高于对照组（p<0.0001）。苏木精和伊红染色显示的嗜酸性粒细胞浸润程度与MBP免疫染色显示的嗜酸性粒细胞浸润和脱颗粒情况相关；然而，在CC组中，免疫荧光显示的嗜酸性粒细胞浸润或脱颗粒与所测量的任何组织学参数之间均未发现其他相关性。
与健康对照者相比，CC患者结肠黏膜中的嗜酸性粒细胞浸润和脱颗粒增加。嗜酸性粒细胞及其细胞毒性颗粒蛋白可能参与CC的发病机制。需要进一步研究以阐明CC中嗜酸性粒细胞激活的机制。
