The University of Texas School of Public Health, Division of Epidemiology, Human Genetics, and Environmental Sciences, Center for Infectious Diseases, Houston, Texas, United States of America.
The University of Texas Medical School, Houston, Texas, United States of America.
PLoS One. 2014 Mar 25;9(3):e93144. doi: 10.1371/journal.pone.0093144. eCollection 2014.
Irritable bowel syndrome (IBS) is one of the most frequently diagnosed disorders, affecting about 20% of the general population in Western countries. This syndrome poses an enormous socio-economic burden, impairs the quality of life substantially, and increases healthcare costs. IBS can be classified as either idiopathic (ID-IBS) with unknown etiology or post-infectious (PI-IBS), which develops after a bout of acute diarrhea or gastroenteritis. Little is known about the immunopathogenesis of these two forms of IBS. We evaluated various biomarkers in clinical samples of ID-IBS and PI-IBS patients with the goal to test the hypothesis that the immunologic presentations of these forms of IBS are similar, despite their apparent different etiologic origins. Sera and stool samples from PI-IBS, ID-IBS, and healthy volunteers were analyzed for relative amounts of 36 different biomarkers using the Proteome Profiler Human Cytokine Array Panel A Kit and quantitative ELISA. Our results demonstrated significantly high levels of chemotactic chemokines monocytes chemotactic protein-1 (CCL2) [p-value = 0.003], macrophage inflammatory protein-1β (CCL4) [p-value = 0.010], and CXCL16 (p-value 0.001) in the sera and stools of both ID-IBS and PI-IBS patients. Furthermore, pro-inflammatory cytokines (IFN-γ, IL-1β, and TNF-α) were significantly higher in IBS patients. Anti-inflammatory cytokines (IL-10, IL-4, and IL-13) were variable except IL-10, which was significantly higher in the healthy volunteers than the IBS patients. Remarkably, the amounts and expression pattern of these biomarkers were not significantly different between ID-IBS and PI-IBS. Thus, ID-IBS and PI-IBS present similar immunologic and clinical phenotypes, in spite of their different etiologic origins.
肠易激综合征(IBS)是最常见的诊断疾病之一,影响约 20%的西方国家普通人群。这种综合征造成了巨大的社会经济负担,极大地降低了生活质量,并增加了医疗保健成本。IBS 可以分为特发性(ID-IBS)和感染后(PI-IBS),前者病因不明,后者在急性腹泻或肠胃炎发作后发展而来。人们对这两种 IBS 的免疫发病机制知之甚少。我们评估了 ID-IBS 和 PI-IBS 患者的临床样本中的各种生物标志物,目的是检验以下假设,即尽管这两种 IBS 的病因明显不同,但它们的免疫表现相似。使用 Proteome Profiler Human Cytokine Array Panel A 试剂盒和定量 ELISA 分析了 PI-IBS、ID-IBS 和健康志愿者的血清和粪便样本中 36 种不同生物标志物的相对含量。我们的结果表明,ID-IBS 和 PI-IBS 患者的血清和粪便中趋化因子单核细胞趋化蛋白-1(CCL2)[p 值 = 0.003]、巨噬细胞炎性蛋白-1β(CCL4)[p 值 = 0.010]和 CXCL16(p 值 0.001)的水平显著升高。此外,IBS 患者的促炎细胞因子(IFN-γ、IL-1β 和 TNF-α)水平显著升高。抗炎细胞因子(IL-10、IL-4 和 IL-13)水平不同,除了 IL-10,健康志愿者中的 IL-10 水平显著高于 IBS 患者。值得注意的是,ID-IBS 和 PI-IBS 之间这些生物标志物的数量和表达模式没有显著差异。因此,尽管病因不同,但 ID-IBS 和 PI-IBS 表现出相似的免疫和临床表型。