Department of Clinical Sciences, Department of Gastroenterology and Nutrition, Lund University, Skåne University Hospital, Malmö, Sweden.
Department of Clinical Sciences, Department of Medicine, Lund University, Skåne University Hospital, Malmö, Sweden.
BMC Immunol. 2022 Jun 6;23(1):29. doi: 10.1186/s12865-022-00504-5.
Collagenous colitis (CC) is a common cause of chronic diarrhea and is characterized by a subepithelial thickened collagen layer in the colonic mucosa. It shares many of the characteristics found in autoimmune diseases, but no autoantibodies have been identified. In CC, an imbalance in collagen turnover is evident. The purpose of the present study was to investigate whether any collagen-associated autoantibodies or other antibodies such as TPO and ASCA were present, and if levels of total IgE were increased.
Sera from women with active CC were analysed with ELISA for detection of autoantibodies against collagen type III and IV (Col III and IV), matrix metalloproteinase-9 (MMP-9), tissue inhibitors of metalloproteinase-1 (TIMP-1) and tenascin-C (TNC). Sera were also analysed for TPO, ASCA and total IgE. Healthy female blood donors served as controls. The cut-off value in the control group was defined as relative units > 97.5th percentile.
Sixty-six women were included (mean age 60 years; range 31-74, mean disease duration 6 years; range 1-22). No autoantibody was significantly overexpressed in the CC population compared to controls. The mean disease duration was lower (p = 0.03) in the subjects who expressed collagen-associated autoantibodies (3.7 years; range 1-14), compared to those who did not (6.4 years; range 1-22). Treatment with budesonide was not associated with any of these autoantibodies.
No increased presence of the investigated antibodies could be found in the present study of CC. Neither could antibodies against ASCA or TPO, or elevated levels of IgE, be found. Consequently, no association was found between CC and these proteins, even though this may not be generalizable to other compounds in the collagen layer.
胶原性结肠炎(CC)是慢性腹泻的常见病因,其特征是结肠黏膜上皮下有增厚的胶原层。它与许多自身免疫性疾病具有相同的特征,但尚未发现自身抗体。在 CC 中,胶原代谢失衡明显。本研究旨在探讨是否存在任何与胶原相关的自身抗体或其他抗体,如 TPO 和 ASCA,以及总 IgE 是否升高。
采用 ELISA 法检测活动期 CC 妇女血清中抗胶原 III 和 IV(Col III 和 IV)、基质金属蛋白酶-9(MMP-9)、金属蛋白酶组织抑制剂-1(TIMP-1)和 tenascin-C(TNC)的自身抗体。还分析了血清中的 TPO、ASCA 和总 IgE。健康女性献血者作为对照。对照组的截断值定义为相对单位>第 97.5 百分位数。
共纳入 66 例女性(平均年龄 60 岁;范围 31-74 岁,平均病程 6 年;范围 1-22 年)。与对照组相比,CC 人群中没有任何自身抗体明显过表达。表达胶原相关自身抗体的患者(3.7 年;范围 1-14 年)的平均病程较短(p=0.03),而未表达胶原相关自身抗体的患者(6.4 年;范围 1-22 年)。布地奈德治疗与这些自身抗体无关。
本研究未发现 CC 患者存在上述抗体增加。也未发现抗 ASCA 或 TPO 抗体或 IgE 水平升高。因此,CC 与这些蛋白之间没有发现关联,尽管这可能不适用于胶原层中的其他化合物。