The Complex Link and Disease Between the Gut Microbiome and the Immune System in Infants

Abstract

The human gut microbiome is important for human health. The development of stable microbial communities in the gastrointestinal tract is closely related to the early growth and development of host immunity. After the birth of a baby, immune cells and the gut microbiome mature in parallel to adapt to the complex gut environment. The gut microbiome is closely linked to the immune system and influences each other. This interaction is associated with various diseases in infants and young children, such as asthma, food allergies, necrotizing colitis, obesity, and inflammatory bowel disease. Thus, the composition of the infant gut microbiome can predict the risk of disease development and progression. At the same time, the composition of the infant gut microbiome can be regulated in many ways and can be used to prevent and treat disease in infants by modulating the composition of the infant gut microbiome. The most important impacts on infant gut microbiota are maternal, including food delivery and feeding. The differences in the gut microbiota of infants reflect the maternal gut microbiota, which in turn reflects the gut microbiota of a given population, which is clinically significant.

Keywords: diseases; immune; infant; maturation; microbiome.

Figure 1

Commensals and pathogens produce different immune responses. PRRs identify MAMPs on pathogens and symbionts and are extensively expressed in intestinal epithelial cells, macrophages, and dendritic cells. Dendritic cells offer antigens to naive T cells as a result of commensals, and these cells differentiate into Treg cells, which emit anti-inflammatory cytokines and spread systemic and local tolerance. Simultaneously, phagocyte migration is inhibited, allowing microbial antigens to reach lymphoid tissue and increasing B- and T-cell activation. Conversely, pathogenic germs cause dendritic cells to secrete pro-inflammatory cytokines, which cause naive T cells to differentiate into Th1 and Th17 cells, resulting in a pro-inflammatory immune response. (Created in BioRender.com).