Impact of maternal infection and breast inflammation on infant growth in Guatemala

Background It is well known that certain maternal infections impair infant growth. Less clear is whether subclinical asymptomatic breast inflammation during the first six months of lactation will also retard infant growth. During subclinical mastitis, a common inflammatory condition of the lactating breast, tight epithelial junctions become “leaky” allowing for movement of sodium and potassium, pro‐inflammatory cytokines, and growth factors into milk via the paracellular pathway. The objectives of this longitudinal study were to: (1) to explore the consequences of maternal infection on infant weight‐for‐age (WAZ), length‐for‐age (LAZ) and head‐circumference‐for‐age (HCZ) at two stages of lactation; (2) and to investigate the relative contribution of milk pro‐inflammatory cytokines and growth factors to infant anthropometry. Methods Breast milk samples were collected from a cohort of lactating Mam ‐Mayan mothers during early (0–6 wks, n=134) and established lactation (4–6 mo, n=120). Inductively Coupled Plasma Mass Spectrometry measured milk Na and K. Luminex measured milk pro‐inflammatory cytokines (IL‐1, IL‐6, IL‐8, TNF‐a) and growth factors (EGF, VEGF). Analysis for presence of maternal urine leukocytes and direct smear of maternal stool samples for non‐pathogenic protozoa ( Blastocystis hominis, Entamoeba coli , Iodamoeba butschli and Endolimax nana ) were measured. Independent variables for breast leakiness (Na/K ratio), breast inflammation, maternal infection and growth factors in milk were explored in separate multiple linear regression models for LAZ, WAZ and HCZ in early and in established lactation. Results Breast leakiness, as measured by a higher Na/K ratio, was positively correlated with all pro‐inflammatory cytokines in early lactation but in established lactation, only milk IL‐6 was positively correlated with Na/K ratio. In early lactation, LAZ was positively associated with maternal height and urine leukocytes. WAZ was positively associated with maternal weight and negatively with milk Na/K ratio and maternal stool Blastocystis hominis. HCZ was also negatively associated with milk Na/K ratio and maternal stool Blastocystis hominis but positively with the pro‐inflammatory cytokine IL‐6 in milk. In established lactation, LAZ was positively associated with maternal height but negatively with maternal stool Entamoeba coli and EGF in milk. WAZ was also negatively associated with maternal stool Entamoeba coli and positively with maternal weight and milk pro‐inflammatory cytokine TFN‐a. HCZ was positively associated with maternal height and the milk pro‐inflammatory cytokine IL‐6 but negatively with EGF in milk. Conclusion Our integrative approach shows that non‐pathogenic protozoa in maternal stool and breast leakiness contribute to poor infant growth. However, in contrast to our expectation that pro‐inflammatory cytokines in milk would retard infant growth and that growth factors would promote infant growth, we observed the opposite to be true which suggests a more complex interrelationship among maternal infection, breast inflammation and infant growth than previously understood. Support or Funding Information McGill University, School of Dietetics and Human Nutrition GREAT award;McGill University, Institute of Parasitology and Centre for Host‐Parasite Interaction Bridging Funds