Immune response changes induced by diabetes are a risk factor for infections during pregnancy and may modify the development of the newborn’s immune system. The present study analyzed colostrum and maternal and cord blood of diabetic women to determine (1) the levels of the cytokines IFN-γ and TGF-β and (2) phagocytic activity after incubation with cytokines. Methods. Colostrum and maternal and cord blood samples were classified into normoglycemic (N = 20) and diabetic (N = 19) groups. Cytokine levels, superoxide release, rate of phagocytosis, bactericidal activity, and intracellular Ca2+ release by phagocytes were analyzed in the samples. Irrespective of glycemic status, IFN-γ and TGF-β levels were not changed in colostrum and maternal and cord blood. In maternal blood and colostrum, superoxide release by cytokine-stimulated phagocytes was similar between the groups. Compared to spontaneous release, superoxide release was stimulated by IFN-γ and TGF-β in normoglycemic and diabetic groups. In the diabetic group, cord blood phagocytes incubated with IFN-γ exhibited higher phagocytic activity in response to EPEC, and maternal blood exhibited lower microbicidal activity. These data suggest that diabetes interferes in maternal immunological parameters and that IFN-γ and TGF-β modulate the functional activity of phagocytes in the colostrum, maternal blood, and cord blood of pregnant diabetic women. 1. Introduction Maternal interaction with the fetus is bidirectional. Fetal and placental tissues require suitable environment, under homeostasis, whereas the maternal body is affected by factors related to metabolic adjustments. In this relationship, the fetus receives passive immunity from the mother, which is crucial for newborn adaptation to the extrauterine environment because it provides protection against infectious agents during the first months of life [1, 2]. Cells with phagocytic and microbicidal activity are among the multiple immune components of blood and human milk that play an important role in child protection [3, 4]. A number of studies report that diabetic patients have low phagocytic and microbicidal activity and reactive oxygen species production due to changes in their antioxidant systems. Moreover, the reduction in phagocytic and microbicidal activity of leukocytes is likely related to an increase in blood glucose levels [5–7]. In diabetic individuals, the balance between proinflammatory and anti-inflammatory cytokines is not fully understood. Some studies show that they prioritize the production of proinflammatory cytokines [8], whereas
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