Institute of Human Genetics, Polish Academy of Sciences, 60-479 Poznan, Poland.
Department of Gastroenterology, Dietetics and Internal Medicine, Poznan University of Medical Sciences, 60-355 Poznan, Poland.
Int J Mol Sci. 2024 Sep 4;25(17):9589. doi: 10.3390/ijms25179589.
Inflammatory bowel disease (IBD) is an incurable, chronic disorder of the gastrointestinal tract whose incidence increases every year. Scientific research constantly delivers new information about the disease and its multivariate, complex etiology. Nevertheless, full discovery and understanding of the complete mechanism of IBD pathogenesis still pose a significant challenge to today's science. Recent studies have unanimously confirmed the association of gut microbial dysbiosis with IBD and its contribution to the regulation of the inflammatory process. It transpires that the altered composition of pathogenic and commensal bacteria is not only characteristic of disturbed intestinal homeostasis in IBD, but also of viruses, parasites, and fungi, which are active in the intestine. The crucial function of the microbial metabolome in the human body is altered, which causes a wide range of effects on the host, thus providing a basis for the disease. On the other hand, human genomic and functional research has revealed more loci that play an essential role in gut homeostasis regulation, the immune response, and intestinal epithelial function. This review aims to organize and summarize the currently available knowledge concerning the role and interaction of crucial factors associated with IBD pathogenesis, notably, host genetic composition, intestinal microbiota and metabolome, and immune regulation.
炎症性肠病（IBD）是一种不可治愈的慢性胃肠道疾病，其发病率逐年增加。科学研究不断提供有关该疾病及其多因素、复杂病因的新信息。然而，要完全发现和理解 IBD 发病机制的完整机制，仍然是当今科学面临的重大挑战。最近的研究一致证实了肠道微生物失调与 IBD 的关联及其对炎症过程的调节作用。事实证明，致病性和共生细菌组成的改变不仅是 IBD 中肠道内稳态紊乱的特征，也是病毒、寄生虫和真菌在肠道中活跃的特征。微生物代谢组在人体中的关键功能发生改变，从而对宿主产生广泛的影响，为疾病提供了基础。另一方面，人类基因组和功能研究揭示了更多在肠道内稳态调节、免疫反应和肠道上皮功能中起重要作用的基因座。本综述旨在组织和总结与 IBD 发病机制相关的关键因素的作用和相互作用的现有知识，特别是宿主遗传组成、肠道微生物群和代谢组以及免疫调节。
