Gut immunity heavily influences susceptibility to infectious and non-communicable diseases. This highlights the need to establish early life factors that shape gut immunity development. Infant nutrition is known to play an important role in gut immune imprinting. Colostrum is the physiological food for the first 2-3 days of life and is extremely rich in biologically active components such as antibodies, growth factors, vitamins, and oligosaccharides. While this composition suggests colostrum is designed to satisfy the needs of the developing newborn, there is a major gap of knowledge on its role in immune development.
To fill this gap of knowledge, we established a unique mouse model of colostrum deprivation where mice were cross-fostered at birth by mothers that were at an advanced stage of lactation and did not provide colostrum anymore. We analysed gut immunity at weaning and found a major decrease in innate lymphoid group 2 and T helper 2 cells in the small intestine of mice deprived of colostrum as compared to physiologically breastfed mice. We further observed a decrease in gut barrier and representation of goblet cells in mice lacking colostrum at birth. We then addressed the impact of abnormal gut development on susceptibility to infection to intestinal helminth parasite, Heligmosomoides polygyrus. Mice deprived of colostrum showed a dramatic increase in susceptibility to infection as shown by the amount of eggs in feces and worms in their intestine.
In conclusion, our data demonstrate that colostrum is critical for type 2 immunity development and suggest that promotion of colostrum feeding is required to prevent parasitic infection in childhood.