BioX Centre and School of Basic Sciences, Indian Institute of Technology Mandi, Mandi, Himachal Pradesh, India.
Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan.
PLoS One. 2020 Mar 24;15(3):e0228358. doi: 10.1371/journal.pone.0228358. eCollection 2020.
Inflammatory bowel disease results from alterations in the immune system and intestinal microbiota. The role of intestinal epithelial cells (IECs) in maintaining gut homeostasis is well known and its perturbation often causes gastrointestinal disorders including IBD. The epithelial specific adaptor protein (AP)-1B is involved in the establishment of the polarity of IECs. Deficiency of the AP-1B μ subunit (Ap1m2-/-) leads to the development of chronic colitis in mice. However, how this deficiency affects the gut microbes and its potential functions remains elusive. To gain insights into the gut microbiome of Ap1m2-/- mice having the colitis phenotype, we undertook shotgun metagenomic sequencing analysis of knockout mice. We found important links to the microbial features involved in altering various physiological pathways, including carbohydrate metabolism, nutrient transportation, oxidative stress, and bacterial pathogenesis (cell motility). In addition, an increased abundance of sulfur-reducing and lactate-producing bacteria has been observed which may aggravate the colitis condition.
炎症性肠病是由免疫系统和肠道微生物群的改变引起的。肠道上皮细胞(IECs)在维持肠道内环境稳定方面的作用是众所周知的,其功能障碍常常导致胃肠道疾病,包括炎症性肠病。上皮细胞特异性衔接蛋白(AP)-1B 参与了 IEC 极性的建立。AP-1B μ 亚基(Ap1m2-/-)的缺失会导致小鼠发生慢性结肠炎。然而,这种缺失如何影响肠道微生物及其潜在功能仍不清楚。为了深入了解具有结肠炎表型的 Ap1m2-/-小鼠的肠道微生物组,我们对敲除小鼠进行了鸟枪法宏基因组测序分析。我们发现了与改变各种生理途径相关的微生物特征的重要联系,包括碳水化合物代谢、营养物质运输、氧化应激和细菌发病机制(细胞运动)。此外,还观察到硫酸盐还原菌和产乳酸菌的丰度增加,这可能加重结肠炎的病情。