Advances in the interaction between intestinal macrophages and the gut microbiota in intestinal diseases

The human body harbors a vast array of microorganisms on its surface, with the intestinal serving as the primary habitat. The gut microbiota comprises thousands of species of bacteria, viruses, fungi, and protozoa, forming a vast and dynamic microbial ecosystem, with intestinal bacteria being the most prominent component. The intestinal mononuclear phagocyte system, as the core component of the intestinal immune system, is positioned at a critical interface between the host and the microbiome. It frequently comes into direct or indirect contact with a large number of foreign antigens and plays a key role in distinguishing between food antigens and commensal bacteria. Intestinal macrophages can differentiate from blood monocytes or originate during embryonic development, and localize to specific tissue niches before birth. These resident intestinal macrophages exhibit significant heterogeneity due to factors such as individual development, tissue location, and functional programming. Consequently, the macrophages display different functional phenotypes depending on their microenvironment. Among these, the gut microbiota play a crucial role in shaping intestinal macrophages directly or indirectly, thereby exerting a significant impact on the occurrence and progression of intestinal diseases. Concurrently, the macrophage immune responses play an important role in shaping microbial communities and molding the microbial ecology to favor host metabolic activities. The interaction between intestinal macrophages and the microbiota plays a significant role in various intestinal diseases, such as inflammatory bowel disease, antibioticassociated colitis, and irritable bowel syndrome. This review predominantly focuses on the origin, characteristics, and function of intestinal macrophages, while also exploring the the advances regarding the interaction between macrophages and the gut microbiota and their roles in the pathogenesis of intestinal diseases.