Exploring the Connections: Autophagy, Gut Microbiota, and Inflammatory Bowel Disease Pathogenesis

Abstract

Inflammatory Bowel Disease (IBD), which includes Crohn's disease and ulcerative colitis, represents a complex and growing global health issue with a multifaceted origin. This review delves into the intricate relationship between gut microbiota, autophagy, and the development of IBD. The gut microbiota, a diverse community of microorganisms, plays a vital role in maintaining gut health, while imbalances in this microbial community, known as dysbiosis, are linked to IBD. Autophagy, a process by which cells recycle their components, is essential for gut homeostasis and the regulation of immune responses. When autophagy is impaired and dysbiosis occurs, they individually contribute to IBD, with their combined impact intensifying inflammation. The interconnectedness of gut microbiota, autophagy, and the host's immune system is central to the onset of IBD. The review also examines how diet influences gut microbiota and its subsequent effects on IBD. It highlights the therapeutic potential of targeting the microbiota and modulating autophagic pathways as treatment strategies for IBD. Understanding these interactions could lead to personalized therapies within the rapidly advancing fields of microbiome research and immunology.

Keywords: Crohn’s disease; autophagy; gut microbiota; inflammatory bowel disease; ulcerative colitis.

Graphical abstract

Figure 1

Gut Microbiota in Healthy and Diseased State. Created with Biorender.com.

Figure 2

Stages of autophagy mechanism. Created with Biorender.com.

Figure 3

Detailed Autophagy Pathway (adapted from KEGG database). ATG16 is a key gene associated with autophagy, specifically involved in autophagosome formation. Single nucleotide polymorphisms (SNPs), specifically rs2241880 and rs6754677 in the ATG16 gene, have been identified in patients with Crohn’s disease. These genetic variations are linked to the onset of CD, indicating a genetic predisposition to altered autophagic processes. The presence of mutations, particularly in the interaction between ATG16 and other autophagy-related genes, can hinder the efficient clearance of CD-associated bacteria from epithelial cells.