Calzadilla Nathan, Qazi Aisha, Sharma Anchal, Mongan Kai, Comiskey Shane, Manne Jahnavi, Youkhana Alvin G, Khanna Sonam, Saksena Seema, Dudeja Pradeep K, Alrefai Waddah A, Gill Ravinder K
Department of Biomedical Engineering, University of Illinois Chicago, Chicago, IL 60612, USA.
Division of Gastroenterology & Hepatology, University of Illinois Chicago, Chicago, IL 60612, USA.
Metabolites. 2023 Jul 23;13(7):873. doi: 10.3390/metabo13070873.
Inflammatory bowel diseases (IBD) involve complex interactions among genetic factors, aberrant immune activation, and gut microbial dysbiosis. While metabolomic studies have focused on feces and serum, fewer investigations have examined the intestinal mucosa despite its crucial role in metabolite absorption and transport. The goals of this study were twofold: to test the hypothesis that gut microbial dysbiosis from chronic intestinal inflammation leads to mucosal metabolic alterations suitable for therapeutic targeting, and to address gaps in metabolomic studies of intestinal inflammation that have overlooked the mucosal metabolome. The chronic DSS colitis was induced for five weeks in 7-9-week-old wild-type C57BL/6J male mice followed by microbial profiling with targeted 16srRNA sequencing service. Mucosal metabolite measurements were performed by Metabolon (Morrisville, NC). The data were analyzed using the bioinformatic tools Pathview, MetOrigin, and Metaboanalyst. The novel findings demonstrated increases in several host- and microbe-derived purine, pyrimidine, endocannabinoid, and ceramide metabolites in colitis. Origin analysis revealed that microbial-related tryptophan metabolites kynurenine, anthranilate, 5-hydroxyindoleacetate, and C-glycosyltryptophan were significantly increased in colon mucosa during chronic inflammation and strongly correlated with disease activity. These findings offer new insights into the pathophysiology of IBD and provide novel potential targets for microbial-based therapeutics.
炎症性肠病(IBD)涉及遗传因素、异常免疫激活和肠道微生物生态失调之间的复杂相互作用。虽然代谢组学研究主要集中在粪便和血清上,但尽管肠黏膜在代谢物吸收和转运中起关键作用,对其进行研究的却较少。本研究有两个目标:检验慢性肠道炎症导致的肠道微生物生态失调会引起适合治疗靶向的黏膜代谢改变这一假设,并填补肠道炎症代谢组学研究中忽视黏膜代谢组的空白。在7至9周龄的野生型C57BL/6J雄性小鼠中诱导慢性葡聚糖硫酸钠(DSS)结肠炎5周,随后使用靶向16srRNA测序服务进行微生物分析。通过Metabolon公司(北卡罗来纳州莫里斯维尔)进行黏膜代谢物测量。使用生物信息学工具Pathview、MetOrigin和Metaboanalyst对数据进行分析。新发现表明,结肠炎中几种宿主和微生物来源的嘌呤、嘧啶、内源性大麻素和神经酰胺代谢物增加。来源分析显示,在慢性炎症期间,结肠黏膜中微生物相关的色氨酸代谢物犬尿氨酸、邻氨基苯甲酸、5-羟基吲哚乙酸和C-糖基色氨酸显著增加,且与疾病活动密切相关。这些发现为IBD的病理生理学提供了新见解,并为基于微生物的治疗提供了新的潜在靶点。