Bellomo Claudia, Mauriello Francesca, Nigro Federica, Passannanti Francesca, Colucci Cante Rosa, Nigro Roberto, Barone Maria Vittoria, Nanayakkara Merlin
Department of Translational Medical Science, Section of Pediatrics, University Federico II, Naples, Italy.
ELFID (European Laboratory for the Investigation of Food Induced Diseases), University Federico II, Naples, Italy.
Front Nutr. 2025 May 13;12:1549120. doi: 10.3389/fnut.2025.1549120. eCollection 2025.
Celiac disease (CeD) is an autoimmune disorder characterized by damage to the small intestine that occurs in genetically predisposed individuals after gluten consumption. Dietary exclusion is the only treatment. Gliadin is one of the main protein component of wheat gluten, and is poorly digested. Undigested peptide, p31-43, triggers several different processes, including inflammation. Intestinal organoids from CeD biopsies are good models for studying CeD inflammation. Postbiotics have been shown to modulate the effects of p31-43 in Caco-2 cells and inflammation in CeD organoids. The aims of this study was to study the anti-inflammatory activity of milk-based postbiotics from of .
Postbiotics from CECT 749-fermented milk enriched with LA (linoleic acid), SCGs (Spent Coffee Grounds) and SCG oil were produced. Gliadin peptide p31-43 was used to induce inflammation on Caco2 cells. Organoids were derived from intestinal biopsies of 3 controls (CTRs) and 3 GCD (gluten containing diet)-CeD patients. NF-kB activation, a marker of inflammation, was evaluated by Western Blot analysis.
The results showed that pretreatment with all milk-based postbiotics of , except for SCG oil, inhibited the activation of NF-kB in the presence of the gliadin peptide in Caco-2 cells. The most efficient postbiotics, namely, milk-based postbiotics of with or without SCGs, could also reduce inflammation in intestinal organoids from CeD patients.
Milk-based postbiotics of , with or without SCGs, prevents the proinflammatory effects of gliadin on Caco-2 cells and constitutive inflammation in CeD intestinal organoids, independent of the CLA (Conjugated linoleic acid) concentration.
乳糜泻(CeD)是一种自身免疫性疾病,其特征是在遗传易感个体摄入麸质后小肠受损。饮食排除是唯一的治疗方法。麦醇溶蛋白是小麦麸质的主要蛋白质成分之一,且消化性差。未消化的肽p31 - 43会引发多种不同过程,包括炎症。来自CeD活检组织的肠道类器官是研究CeD炎症的良好模型。已证明后生元可调节p31 - 43在Caco - 2细胞中的作用以及CeD类器官中的炎症。本研究的目的是研究源自[具体来源未明确]的基于牛奶的后生元的抗炎活性。
制备了富含亚油酸(LA)、咖啡渣(SCGs)和咖啡渣油的CECT 749发酵乳中的后生元。使用麦醇溶蛋白肽p31 - 43在Caco2细胞上诱导炎症。类器官源自3名对照(CTRs)和3名麸质含饮食(GCD)-CeD患者的肠道活检组织。通过蛋白质印迹分析评估炎症标志物核因子κB(NF - kB)的激活情况。
结果表明,除咖啡渣油外,所有源自[具体来源未明确]的基于牛奶的后生元预处理均能在Caco - 2细胞中存在麦醇溶蛋白肽的情况下抑制NF - kB的激活。最有效的后生元,即含或不含咖啡渣的源自[具体来源未明确]的基于牛奶的后生元,也可减轻CeD患者肠道类器官中的炎症。
含或不含咖啡渣的源自[具体来源未明确]的基于牛奶的后生元可预防麦醇溶蛋白对Caco - 2细胞的促炎作用以及CeD肠道类器官中的固有炎症,与共轭亚油酸(CLA)浓度无关。