The effect of feeding patterns on serum zonulin levels in infants at 3-4 months of age.

Zonulin so far is the only known endogenous modulator of intercellular tight junctions which regulate the intestinal permeability. Breastfeeding is considered to enhance the integrity of the gastrointestinal tract; however, limited data are available about the effect of feeding patterns on intestinal permeability. We aimed to investigate the potential association between the mode of feeding (breast versus formula milk) and the serum zonulin levels as a marker of intestinal permeability. One hundred fifty-seven full-term, healthy infants, born after an uncomplicated pregnancy, were enrolled within 72-96 h of life. Blood samples from 105 infants were obtained at 3 to 4 months of life. Serum zonulin levels were measured by ELISA. Out of 105 infants, 52.4% (55) were female, and 58.1% (61) were delivered by caesarian section at a mean gestational age of 38.9 (SD ± 1.0) weeks. At the time of blood sampling, median age was 3.4 (IQR 3.20-3.50) months, and mean weight was 6332 (SD ± 692) gr. Infants were divided in three groups according to the feeding patterns: exclusive breastfeeding (n = 42), mixed feeding (n = 41), and cow's milk formula (n = 22). The feeding pattern had no impact on infants' serum zonulin levels. Moreover, zonulin levels were not affected by infant's clinical and epidemiological characteristics such as body weight or family history of autoimmune disease.Conclusion: In our study, different feeding patterns were not associated with serum zonulin levels in healthy infants at 3-4 months of age. What is Known: • Serum zonulin is upregulated in conditions with increased intestinal permeability • Breast milk favors the physiological decline of the intestinal permeability after birth in the neonates What is New: • Serum zonulin levels were not affected by the feeding pattern (breast milk versus formula) in infants at 3-4 months of age • Clinical and epidemiological characteristics of infants had no impact on zonulin levels.

Breastmilk cell trafficking induces microchimerism-mediated immune system maturation in the infant.

Initiating breastfeeding within the first hour of life confers an important benefit in terms of child mortality and severe morbidity. Intestinal permeability to ingested macromolecules and immunoglobulins is limited to the first days of human life. These exchanges cease in the very early post-partum period but may increase beyond the neonatal period in response to local inflammation or introduction of a weaning food. From animal- and limited human-based observations, compelling evidence points out to breastmilk cells also trafficking from mother to infant mucosal tissues and participating to the maternal microchimerism. The precise nature of breastmilk cells that are involved is presently not known but likely includes progenitor/stem cells-representing up to 6% of breastmilk cells-with possible contribution of mature immune cells. Stem cell microchimerism may induce tolerance to non-inherited maternal antigens (NIMAs), breastfeeding generating regulatory T cells (Treg ) that suppress antimaternal immunity. Therefore, in complement to pregnancy-induced microchimerism, breastfeeding-induced microchimerism may be pivotal in infant immune development, intestinal tissue repair/growth and protection against infectious diseases. As a continuum of the gestational period, the neonatal gut may be considered as a temporary, but important developmental extension of the role played by the placenta during intrauterine life; breastmilk playing the role of maternal blood by delivering maternal soluble factors (macromolecules, Ig, cytokines) and immunologically active milk cells. A better understanding of breastfeeding-induced maternal microchimerism would provide further evidence in support of public health messages that reinforce the importance of early initiation of breastfeeding.