2017年3月8日， 國際頂尖學術期刊《Science》旗下《 Science Translational Medicine》雜誌上線上發表了美國猶他大學醫學院June L. Round研究組的一篇研究論文， 研究報告稱存在於腸道中的一種酵母菌可能會加劇克隆氏病(Crohn’s Disease)， 而阻斷該真菌在腸道中引起問題可令某些炎性腸病患者的症狀減輕。
目前大約有160萬名美國人罹患炎性腸病(IBD)， 每年新診斷的病例多達7萬人。 儘管許多患者用抗炎藥物來控制症狀， 但IBD無法治癒。 儘管有若干研究闡明了腸道細菌與IBD之間的瓜葛， 但對其它腸道微生物與IBD的關係則鮮有關注， 儘管有近七成的克隆氏病(CD)患者往往會對酵母菌發起免疫反應。
與腸道中沒有定植酵母菌的小鼠(左， 對照組)或腸道中被不同酵母菌株定植的小鼠相比， 腸道中定植了酵母菌(中)的小鼠會出現更嚴重的炎性腸病所致的腸道損傷。
原文連結：
原文摘要：
The commensal microbiota has an important impact on host health, which is only beginning to be elucidated. Despite the presence of fungal, archaeal, and viral members, most studies have focused solely on the bacterial microbiota. Antibodies against the yeast Saccharomyces cerevisiae are found in some patients with Crohn’s disease (CD), suggesting that the mycobiota may contribute to disease severity. We report that S. cerevisiae exacerbated intestinal disease in a mouse model of colitis and increased gut barrier permeability. Transcriptome analysis of colon tissue from germ-free mice inoculated with S. cerevisiae or another fungus, Rhodotorula aurantiaca, revealed that S. cerevisiae colonization affected the intestinal barrier and host metabolism. A fecal metabolomics screen of germ-free animals demonstrated that S. cerevisiaecolonization enhanced host purine metabolism, leading to an increase in uric acid production. Treatment with uric acid alone worsened disease and increased gut permeability. Allopurinol, a clinical drug used to reduce uric acid, ameliorated colitis induced by S. cerevisiae in mice. In addition, we found a positive correlation between elevated uric acid and anti-yeast antibodies in human sera. Thus, yeast in the gut may be able to potentiate metabolite production that negatively affects the course of inflammatory bowel disease.