Sharma Bharti, Agriantonis George, Twelker Kate, Ebelle Danielle, Kiernan Samantha, Siddiqui Maham, Soni Aditi, Cheerasarn Sittha, Simon Whenzdjyny, Jiang Winston, Cardona Angie, Chapelet Jessica, Agathis Alexandra Z, Gamboa Alejandro, Dave Jasmine, Mestre Juan, Bhatia Navin D, Shaefee Zahra, Whittington Jennifer
Department of Surgery, NYC Health and Hospitals-Elmhurst, New York, NY 11373, USA.
Department of Surgery, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
Int J Mol Sci. 2025 Mar 11;26(6):2503. doi: 10.3390/ijms26062503.
Inflammatory bowel disease (IBD), encompassing Crohn's disease (CD), ulcerative colitis (UC), and IBD unclassified (IBD-U), is a complex intestinal disorder influenced by genetic, environmental, and microbial factors. Recent evidence highlights the gut microbiota as a pivotal biomarker and modulator in IBD pathogenesis. Dysbiosis, characterized by reduced microbial diversity and altered composition, is a hallmark of IBD. A consistent decrease in anti-inflammatory bacteria, such as , and an increase in pro-inflammatory species, including , have been observed. Metabolomic studies reveal decreased short-chain fatty acids (SCFAs) and secondary bile acids, critical for gut homeostasis, alongside elevated pro-inflammatory metabolites. The gut microbiota interacts with host immune pathways, influencing morphogens, glycosylation, and podoplanin (PDPN) expression. The disruption of glycosylation impairs mucosal barriers, while aberrant PDPN activity exacerbates inflammation. Additionally, microbial alterations contribute to oxidative stress, further destabilizing intestinal barriers. These molecular and cellular disruptions underscore the role of the microbiome in IBD pathophysiology. Emerging therapeutic strategies, including probiotics, prebiotics, and dietary interventions, aim to restore microbial balance and mitigate inflammation. Advanced studies on microbiota-targeted therapies reveal their potential to reduce disease severity and improve patient outcomes. Nevertheless, further research is needed to elucidate the bidirectional interactions between the gut microbiome and host immune responses and to translate these insights into clinical applications. This review consolidates current findings on the gut microbiota's role in IBD, emphasizing its diagnostic and therapeutic implications, and advocates for the continued exploration of microbiome-based interventions to combat this debilitating disease.
炎症性肠病（IBD）包括克罗恩病（CD）、溃疡性结肠炎（UC）和未分类的IBD（IBD-U），是一种受遗传、环境和微生物因素影响的复杂肠道疾病。最近的证据表明，肠道微生物群是IBD发病机制中的关键生物标志物和调节因子。以微生物多样性降低和组成改变为特征的生态失调是IBD的一个标志。已观察到抗炎细菌（如 ）持续减少，而促炎物种（包括 ）增加。代谢组学研究表明，对肠道稳态至关重要的短链脂肪酸（SCFAs）和次级胆汁酸减少，同时促炎代谢物升高。肠道微生物群与宿主免疫途径相互作用，影响形态发生素、糖基化和血小板淋巴管生成素（PDPN）表达。糖基化的破坏会损害粘膜屏障，而异常的PDPN活性会加剧炎症。此外，微生物改变会导致氧化应激，进一步破坏肠道屏障的稳定性。这些分子和细胞的破坏突出了微生物群在IBD病理生理学中的作用。新兴的治疗策略，包括益生菌、益生元和饮食干预，旨在恢复微生物平衡并减轻炎症。针对微生物群的治疗的深入研究表明它们有降低疾病严重程度和改善患者预后的潜力。然而，仍需要进一步研究以阐明肠道微生物群与宿主免疫反应之间的双向相互作用，并将这些见解转化为临床应用。这篇综述整合了关于肠道微生物群在IBD中作用的当前研究结果，强调其诊断和治疗意义，并倡导继续探索基于微生物群的干预措施来对抗这种使人衰弱的疾病。
