Introduction The young piglet is a valuable model for human infants in studies designed to identify interactions between the developing immune system, metabolism and the microbiome in early life. The early postnatal environment, including factors such as weaning and acquisition of the gut microbiota, has been causally linked to the development of later immunological diseases such as allergy and autoimmunity. Here, we show that early-life environment influences development of metabolic and immune phenotype as well as the gut microbiota in a porcine model.
Method Piglets were removed to an isolator facility 24 h after birth, formula fed until 21d at which point they were weaned. Animals were gender and litter-matched to the control group or supplemented with the human probioticBifidobacterium lactis NCC2818 from 1d. Animals were sacrificed at 35d and the experiment was repeated with a second batch of piglets under identical husbandry conditions.
Metabolic profiling of serum and urine at 35d was carried out using 1H Nuclear Magnetic Resonance spectroscopy (NMR). Intestinal barrier function was assessed using immunofluorescence histology and immunoglobulin and cytokine production from various immunological sites was quantified. 16s pyrosequencing was conducted on colonic content and mucosal scrapings.
Results The immediate environment during the first 24 h of life influenced the early microbiota, with animals from different batches having significantly different colonic bacteria and urinary metabolic profiles at 35d. Despite the underlying differences between the experimental batches, the administration of Bifidobacterium lactisNCC2818 in the diet significantly affected the metabolic phenotype, mucosal cytokine and immunogobulin production, and increased expression of intestinal tight cell junction proteins. Importantly, changes in composition of the microbiota were insufficient to explain the effect of the probiotic on these parameters.
Conclusion We demonstrate that the environment during the first day of life influences development of the microbiota, metabolic phenotype and immune parameters and suggest that nutritional intervention at this early stage of life could be beneficial for at-risk infants who have suffered aberrant initial intestinal colonisation caused by, for example, caesarean or premature birth.
Disclosure of interest None Declared.