Patterns of Early-Life Gut Microbial Colonization during Human Immune Development: An Ecological Perspective

Abstract

Alterations in gut microbial colonization during early life have been reported in infants that later developed asthma, allergies, type 1 diabetes, as well as in inflammatory bowel disease patients, previous to disease flares. Mechanistic studies in animal models have established that microbial alterations influence disease pathogenesis via changes in immune system maturation. Strong evidence points to the presence of a window of opportunity in early life, during which changes in gut microbial colonization can result in immune dysregulation that predisposes susceptible hosts to disease. Although the ecological patterns of microbial succession in the first year of life have been partly defined in specific human cohorts, the taxonomic and functional features, and diversity thresholds that characterize these microbial alterations are, for the most part, unknown. In this review, we summarize the most important links between the temporal mosaics of gut microbial colonization and the age-dependent immune functions that rely on them. We also highlight the importance of applying ecology theory to design studies that explore the interactions between this complex ecosystem and the host immune system. Focusing research efforts on understanding the importance of temporally structured patterns of diversity, keystone groups, and inter-kingdom microbial interactions for ecosystem functions has great potential to enable the development of biologically sound interventions aimed at maintaining and/or improving immune system development and preventing disease.

Maternal IgG impairs the maturation of offspring intrathymic IL‐17‐producing γδT cells: Implications for murine and human allergies

“…Microbial factors have a strong impact on the development of immune cells, including CD8 + T cells, B cells, invariant natural killer T (iNKT) cells and γδ T cells . In addition to the neonatal microbiome, antigens encountered by the future mother, such as allergens, may also influence the immune status of the offspring by potentially modulating their T‐cell maturation . In fact, previous reports have demonstrated that maternal allergen immunization prevents neonatal allergy development .…”

“…[7][8][9] In addition to the neonatal microbiome, antigens encountered by the future mother, such as allergens, may also influence the immune status of the offspring by potentially modulating their T-cell maturation. 10,11 In fact, previous reports have demonstrated that maternal allergen immunization prevents neonatal allergy development. [12][13][14][15][16] Several hypotheses exist to explain the impaired allergic responses of offspring.…”

Association of autophagy status with amount of Fusobacterium nucleatum in colorectal cancer

“…Moreover, invasive F. nucleatum is persistently associated with distant metastases from primary colorectal cancers [45]. In contrast, the members of Bifidobacterium genus have been considered to inhibit colorectal carcinogenesis through the prevention of enteropathogenic infection and the inhibition of secondary bile acid production [46][47][48]. Our previous population-based study has shown that intratumoural Bifidobacterium genus may reflect loss of intestinal barrier function in poorly differentiated colorectal cancer [36].…”

Personalized medicine—concepts, technologies, and applications in inflammatory skin diseases

“…In addition, higher microbial endotoxin exposure from farm animals was associated with protection against development of allergy, as suggested in the ‘Eat Dirt’ article by Weiss . Finally, because the gut microbiome is important for the prenatal–early‐life maturation of our immune system , it has been intensively studied in relation to allergic diseases, and perturbations in the infant gut microbiome have been linked to the risk of developing AD . However, several probiotic and prebiotic intervention trials have been conducted, and although some protective effect against AD was observed, the differences were small, and no clear gut microbiome–AD association could be demonstrated .…”