Rafael Souza Pessoa

Pregnancy complicated by obesity is associated with adverse triggered gestational and neonatal outcomes, with reductions in the subtypes of CD4+ T-lymphocytes representing the modulators of inflammation. It needs to be better established how maternal nutritional statuses impact the neuroendocrine–immune system’s action and affect the immunological mechanisms of the maternal–infant relationship via breastfeeding. This study examined the effects of maternal obesity on human colostrum lymphocytes and the intracellular mechanisms of lymphocyte modulation in the presence of leptin, adiponectin, and melatonin via cell proliferation; the release of intracellular calcium; and apoptosis induction. This cross-sectional study analyzed colostrum samples from 52 puerperal splits and divided them into overweight and eutrophic groups. Colostrum lymphocytes underwent immunophenotyping and cell proliferation by flow cytometry and intracellular calcium release and apoptosis assays by immunofluorescence in the presence or absence of hormones. Significant differences were considered when p < 0.05 by the chi-square or t-test. Maternal obesity reduced the population of T-lymphocytes and TCD4+ in human colostrum and proliferative activities (p < 0.05). These hormones restore lymphocyte proliferation to a level similar to the eutrophic group (p < 0.05). Leptin, adiponectin, melatonin hormones, and biological actions consolidated in the scientific literature also represent maternal and infant protection mechanisms via colostrum and the modulation of human colostrum lymphocytes.

Background and objectives: Breastfeeding promotion is an important public health strategy for counter-balancing the negative effects of maternal overweight and obesity. Colostrum contains melatonin, which can attenuate the impacts of excessive maternal weight and boost the infant’s immune system. Therefore, the objective of this study was to analyze the effects of melatonin on mononuclear (MN) phagocytes from the colostrum of women with pre-gestational obesity. Materials and Methods: Colostrum samples were collected postpartum from 100 women at a public hospital in São Paulo, Brazil. The donors were divided into two groups: the control group and the high body mass index (BMI) group. Melatonin levels in the colostrum were determined by an ELISA Kit, and the functional activity of MN cells was assessed using the phagocytosis assay by flow cytometry, and reactive oxygen species (ROS), intracellular calcium, and apoptosis were assessed by fluorimetry using a microplate reader. Results: The colostrum of mothers with pre-gestational high BMI exhibited higher melatonin levels (p < 0.05) and lower phagocytosis (p < 0.05) and ROS release (p < 0.05). Superoxide release was similar between the normal and high BMI groups (p > 0.05). Intracellular calcium release and apoptosis were also higher in the high BMI group (p < 0.05). Melatonin levels likely increased the phagocytosis rate and reduced intracellular calcium release and the apoptosis index (p < 0.05). Conclusions: The results suggest that melatonin is a possible mechanism for maternal–infant protection against obesity and restores the functional activity of colostrum phagocytes in obese mothers.

Adiponectin and leptin play roles in the hunger response, and they can induce the inflammatory process as the initial mechanism of the innate immune response. It is possible for alterations in the levels of these adipokines to compromise the functional activity of human colostrum phagocytes. Therefore, the objective of this study is to analyze the effects of adiponectin and leptin on colostrum mononuclear (MN) cells. Colostrum was collected from 80 healthy donors, who were divided into two groups: the control group and the high body mass index (BMI) group. MN cells were used to analyze phagocytosis by flow cytometry, and reactive oxygen species (ROS), intracellular calcium, and apoptosis were assessed by fluorimetry using a microplate reader. Adipokines restored the levels of phagocytosis to the high BMI group (p < 0.05), with a mechanism that is action-dependent on the release of ROS and intracellular calcium. However, adiponectin and leptin simultaneously contributed to better microbicidal activity, thus reflecting an increase in the apoptosis level (p < 0.05) in the high BMI group. Probably, the maintenance of the balance between adiponectin and leptin levels enhances the protection and decreases the indices of neonatal infection in the breastfeeding infants of women with high BMI values. Therefore, policies that support pre-gestational weight control should be encouraged.

Entamoeba histolytica (E. histolytica) causes amoebiasis, which is a disease with significant morbidity and mortality. Phagocytic cells and cytokines appear to be important in amoebiasis, but very little is known about the influence of these cells and cytokines in protozoan infections. The aim of this study was to analyse the supernatant of cultures of mononuclear (MN) cells with E. histolytica to determine: 1) the levels of the cytokines IFN-γ and TGF-β, and 2) the amoebicidal activity of MN cells after incubation with cytokines. Blood samples were collected from 30 volunteer donors. The cytokine concentrations in MN cells culture supernatants, superoxide release, leukophagocytosis, amoebicide activity, intracellular calcium release and apoptosis were analysed. The IFN-γ concentrations were 6.22 ± 0.36 and TGF-β concentrations were 17.01 ± 2.21 in cells–trophozoite culture supernatants. MN cells, independently of cytokines, in the presence of amoeba increase the superoxide release. In the absence of cytokines, the ingestion of MN cells by amoebae was higher. In the presence of IFN- γ or TGF- β, a lower ingestion of MN cells was observed by amoebae. MN cells treated with cytokines exhibited higher amoebicide and apoptosis indexes. The incubation of cytokines increased the intracellular calcium release by MN cells. These results suggest that cytokines play a beneficial role for the host by activating MN cells against E. histolytica. The increased death of amoebae during the leukophagocytosis suggests that both cytokines (IFN-γ and TGF-β) can modulate the functional activity of MN cells and that these cytokines probably are important in the control of amoebic infections.