Caminero Alberto, Nistal Esther, Herrán Alexandra R, Pérez-Andrés Jénifer, Ferrero Miguel A, Vaquero Ayala Luis, Vivas Santiago, Ruiz de Morales José M G, Albillos Silvia M, Casqueiro Francisco Javier
1Instituto de Biología Molecular,Genómica y Proteómica (INBIOMIC),Campus de Vegazana,Universidad de León,León 24071,Spain.
2Área de Microbiología, Facultad de Biología y Ciencias Ambientales,Universidad de León,León 24071,Spain.
Br J Nutr. 2015 Oct 28;114(8):1157-67. doi: 10.1017/S0007114515002767.
Coeliac disease (CD) is an immune-mediated enteropathy resulting from exposure to gluten in genetically predisposed individuals. Gluten proteins are partially digested by human proteases generating immunogenic peptides that cause inflammation in patients carrying HLA-DQ2 and DQ8 genes. Although intestinal dysbiosis has been associated with patients with CD, bacterial metabolism of gluten has not been studied in depth thus far. The aim of this study was to analyse the metabolic activity of intestinal bacteria associated with gluten intake in healthy individuals, CD patients and first-degree relatives of CD patients. Faecal samples belonging to twenty-two untreated CD patients, twenty treated CD patients, sixteen healthy volunteers on normal diet, eleven healthy volunteers on gluten-free diet (GFD), seventy-one relatives of CD patients on normal diet and sixty-nine relatives on GFD were tested for several proteolytic activities, cultivable bacteria involved in gluten metabolism, SCFA and the amount of gluten in faeces. We detected faecal peptidasic activity against the gluten-derived peptide 33-mer. CD patients showed differences in faecal glutenasic activity (FGA), faecal tryptic activity (FTA), SCFA and faecal gluten content with respect to healthy volunteers. Alterations in specific bacterial groups metabolising gluten such as Clostridium or Lactobacillus were reported in CD patients. Relatives showed similar parameters to CD patients (SCFA) and healthy volunteers (FTA and FGA). Our data support the fact that commensal microbial activity is an important factor in the metabolism of gluten proteins and that this activity is altered in CD patients.
乳糜泻（CD）是一种免疫介导的肠病，由遗传易感性个体接触麸质引起。麸质蛋白被人类蛋白酶部分消化，产生免疫原性肽，导致携带HLA - DQ2和DQ8基因的患者发生炎症。尽管肠道菌群失调与CD患者有关，但迄今为止，麸质的细菌代谢尚未得到深入研究。本研究的目的是分析健康个体、CD患者以及CD患者一级亲属中与麸质摄入相关的肠道细菌的代谢活性。对22名未经治疗的CD患者、20名接受治疗的CD患者、16名正常饮食的健康志愿者、11名无麸质饮食（GFD）的健康志愿者、71名正常饮食的CD患者亲属以及69名采用GFD的CD患者亲属的粪便样本进行了几种蛋白水解活性、参与麸质代谢的可培养细菌、短链脂肪酸（SCFA）以及粪便中麸质含量的检测。我们检测到针对麸质衍生肽33聚体的粪便肽酶活性。与健康志愿者相比，CD患者在粪便麸质酶活性（FGA）、粪便胰蛋白酶活性（FTA）、SCFA和粪便麸质含量方面存在差异。在CD患者中报告了代谢麸质的特定细菌群（如梭菌属或乳杆菌属）的改变。亲属的参数与CD患者（SCFA）和健康志愿者（FTA和FGA）相似。我们的数据支持这样一个事实，即共生微生物活性是麸质蛋白代谢的一个重要因素，并且这种活性在CD患者中发生了改变。
