Sultan Salma, El-Mowafy Mohammed, Elgaml Abdelaziz, Ahmed Tamer A E, Hassan Hebatoallah, Mottawea Walid
Faculty of Health Sciences, School of Nutrition Sciences, University of Ottawa, Ottawa, ON, Canada.
Department of Microbiology and Immunology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt.
Front Physiol. 2021 Sep 27;12:715506. doi: 10.3389/fphys.2021.715506. eCollection 2021.
Inflammatory bowel diseases (IBD) are chronic medical disorders characterized by recurrent gastrointestinal inflammation. While the etiology of IBD is still unknown, the pathogenesis of the disease results from perturbations in both gut microbiota and the host immune system. Gut microbiota dysbiosis in IBD is characterized by depleted diversity, reduced abundance of short chain fatty acids (SCFAs) producers and enriched proinflammatory microbes such as adherent/invasive and HS producers. This dysbiosis may contribute to the inflammation through affecting either the immune system or a metabolic pathway. The immune responses to gut microbiota in IBD are extensively discussed. In this review, we highlight the main metabolic pathways that regulate the host-microbiota interaction. We also discuss the reported findings indicating that the microbial dysbiosis during IBD has a potential metabolic impact on colonocytes and this may underlie the disease progression. Moreover, we present the host metabolic defectiveness that adds to the impact of symbiont dysbiosis on the disease progression. This will raise the possibility that gut microbiota dysbiosis associated with IBD results in functional perturbations of host-microbiota interactions, and consequently modulates the disease development. Finally, we shed light on the possible therapeutic approaches of IBD through targeting gut microbiome.
炎症性肠病(IBD)是一种以反复出现胃肠道炎症为特征的慢性疾病。虽然IBD的病因尚不清楚,但该疾病的发病机制是由肠道微生物群和宿主免疫系统的紊乱引起的。IBD中的肠道微生物群失调表现为多样性减少、短链脂肪酸(SCFA)产生菌丰度降低以及促炎微生物(如黏附/侵袭性细菌和产HS细菌)增多。这种失调可能通过影响免疫系统或代谢途径而导致炎症。IBD中对肠道微生物群的免疫反应已得到广泛讨论。在本综述中,我们重点介绍了调节宿主-微生物群相互作用的主要代谢途径。我们还讨论了已报道的研究结果,这些结果表明IBD期间的微生物失调对结肠细胞具有潜在的代谢影响,这可能是疾病进展的基础。此外,我们还介绍了宿主代谢缺陷,这增加了共生菌失调对疾病进展的影响。这将增加与IBD相关的肠道微生物群失调导致宿主-微生物群相互作用功能紊乱,进而调节疾病发展的可能性。最后,我们阐述了通过靶向肠道微生物群治疗IBD的可能方法。