Spatial and temporal key steps in early‐life intestinal immune system development and education

Abstract

Education of our intestinal immune system early in life strongly influences adult health. This education strongly relies on series of events that must occur in well-defined time windows. From initial colonization by maternalderived microbiota during delivery to dietary changes from mother's milk to solid foods at weaning, these early-life events have indeed long-standing consequences on our immunity, facilitating tolerance to environmental exposures or, on the contrary, increasing the risk of developing noncommunicable diseases such as allergies, asthma, obesity, and inflammatory bowel diseases. In this review, we provide an outline of the recent advances in our understanding of these events and how they are mechanistically related to intestinal immunity development and education. First, we review the susceptibility of neonates to infections and inflammatory diseases, related to their immune system and microbiota changes. Then, we highlight the maternal factors involved in protection and education of the mucosal immune system of the offspring, the role of the microbiota, and the nature of neonatal immune system until weaning. We also present how the development of some immune responses is intertwined in temporal and spatial windows of opportunity. Finally, we discuss pending questions regarding the neonate particular immune status and the activation of the intestinal immune system at weaning.

Probiotics induce intestinal IgA secretion in weanling mice potentially through promoting intestinal APRIL expression and modulating the gut microbiota composition

“…7,8 The complex nutritional components in solid foods at the time of weaning promote the diversification of the intestinal microbiota and trigger the maturation of the mucosal immune system, particularly leading to the production of endogenous IgA. 9,10 The intestinal microbiota at the time of weaning can induce strong immune responses, and inhibition of this process can lower IgA levels, thereby driving susceptibility to intestinal infections, colitis, and other diseases. 11,12 The close relationship between the intestinal microbiota and the production of intestinal IgA provides a potential avenue for microbial interventions to induce the production of endogenous IgA in the gut.…”

Antibiotic use during pregnancy is linked to offspring gut microbial dysbiosis, barrier disruption, and altered immunity along the gut–lung axis

“…In addition to soluble molecules, gut immune cells can also contribute to gut permeability in the inflamed intestine during microbial dysbiosis. Of particular interest in this regard are the ILCs, the innate counterparts of T cells that participate in the establishment of mucosal immunity [27]. Intestinal ILC populations in mice increase significantly 2–4 weeks after birth, corresponding to the rise in intestinal microbiota diversity that occurs during the weaning process [28].…”

Revisiting the steps of Salmonella gut infection with a focus on antagonistic interbacterial interactions

“…It is influenced by host diet, immune system development, and priority effect—a phenomenon in which the order and timing of colonization determine the assembly of microbial communities (usually the species arriving first are favored) [7–9]. The assembly starts by the contact with the maternal microbiota during birth and continues through transitions until it stabilizes in adulthood [10,11]. After reaching homeostasis, the microbial community maintains a more or less stable composition [2,12].…”