Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390.
Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390; and.
J Immunol. 2020 Apr 15;204(8):2277-2284. doi: 10.4049/jimmunol.1701478. Epub 2020 Mar 13.
Inflammatory bowel diseases are associated with complex shifts in microbiota composition. However, it remains unclear whether specific subsets of commensal bacteria induce inflammatory bowel diseases in genetically susceptible hosts. In this study, we found that deficiency of the E3 ligase Itch, which leads to spontaneous colitis and rectal prolapse, is associated with alteration of the gut microbiota. 16S rRNA sequencing showed expansion of colitogenic sp. in Itch mice. Treatment with broad-spectrum antibiotics substantially reduced colonic inflammation in Itch mice. Microbiota of Itch mice failed to induce spontaneous colitis upon transfer to Itch mice but aggravated chemically induced colitis. Furthermore, we found that , which is expanded in Itch mice, was sufficient to induce colon inflammation in Itch mice.
炎症性肠病与微生物群落组成的复杂变化有关。然而，尚不清楚是否特定的共生菌亚群在遗传易感宿主中诱导炎症性肠病。在这项研究中，我们发现 E3 连接酶 Itch 的缺失会导致自发性结肠炎和直肠脱垂，这与肠道微生物群的改变有关。16S rRNA 测序显示，Itch 小鼠中结肠炎相关 sp. 的扩张。广谱抗生素治疗可显著减轻 Itch 小鼠的结肠炎症。Itch 小鼠的微生物群不能在转移到 Itch 小鼠后诱导自发性结肠炎，但会加重化学诱导的结肠炎。此外，我们发现，在 Itch 小鼠中扩张的，足以在 Itch 小鼠中诱导结肠炎症。
