Obesity in pregnancy is associated with systemic inflammation, immunological changes and adverse maternal-fetal outcomes. Information on the association between maternal obesity and breast milk composition is scarce. This study describes changes and relationships between biochemical and immunological parameters of colostrum and serum of overweight and obese women. Colostrum and blood samples were collected from 25 normal weight, 24 overweight and 19 obese women for determination of glucose, total protein, triglycerides, cholesterol, immunoglobulins, complement proteins (C3 and C4), fat and calorie content and C-reactive protein (CRP). Glucose was higher in colostrum of obese women (p = .002). In normal weight and obese women, total protein content was higher in colostrum than in serum (p = .001). Serum triglycerides (p = .008) and cholesterol (p = .010) concentrations were significantly higher in overweight and obese women than in their normal weight counterparts, but in colostrum their concentrations were similar across the three groups. Secretory IgA (sIgA) in colostrum and IgA in serum concentrations were significantly higher (p = .001) in overweight and obese mothers, whereas IgG and IgM concentrations did not vary among the groups (p = .825). Serum C3 (p = .001) and C4 (p = .040) concentrations were higher in obese women. No differences in colostrum complement proteins were detected among the groups. Calorie content (p = .003) and fat (p = .005) concentrations in colostrum and serum CRP (p = .002) were higher in obese women. The results corroborate the hypothesis that colostrum of overweight and obese women undergoes biochemical and immunological changes that affect its composition, namely increasing glucose concentrations, calorie content, fat and sIgA concentrations.

This study sought to determine the chronobiological variations in soluble and cellular components of human breast milk. The material was collected from 36 mothers at three stages of maturity – 3 days (colostrum), 10 days (transitional milk) and 30 days (mature milk) postpartum – and at two times of day – diurnal (12:00 h) and nocturnal (24:00 h) – making a total of 216 samples. Fat and calorie content, antibody concentration, C3 and C4 proteins of the complement system, superoxide anion release by milk mononuclear (MN) and polymorphonuclear (PMN) phagocytes, and concentration of the superoxide dismutase enzyme (CuZn-SOD) were determined. No difference in fat concentration was found between milk collected at the different times or between milk maturation stages but in the transitional milk the calorie concentration was higher in the nocturnal period. IgA was higher in milk collected in the diurnal period regardless of milk maturation. IgG and IgM were at higher concentrations in the diurnal period for both transitional and mature milk. The C3 protein increased significantly in the diurnal period regardless of milk maturation, and the C4 protein increased significantly during the diurnal period in the colostrum and transitional milk stages. Mature milk MN phagocytes had the highest superoxide during the diurnal period. Superoxide release by PMN phagocytes was higher in colostrum and mature milk collected in the diurnal period. CuZn-SOD increased significantly in diurnal and nocturnal colostrum. This chronobiological variation during the first month postpartum may represent an additional breastfeeding mechanism to improve adaptation to environmental changes and establish biological rhythms in the temporal synchronization process.

Breastfeeding and its Relationship with Reduction of Breast Cancer: A Review Breast cancer;breastfeeding;breast milk;alpha-lactalbumin; In this review, we describe the patterns of known immunological components in breast milk and examine the relationship between breastfeeding and reduced risk of breast cancer. The top risk factors for breast cancer are a woman's age and family history, specifically having a first-degree relative with breast cancer. Women that have a history of breastfeeding have been shown to have reduced rates of breast cancer. Although the specific cause has not been elucidated, previous studies have suggested that breastfeeding reduces the risk of breast cancer primarily through two mechanisms: the differentiation of breast tissue and reduction in the lifetime number of ovulatory cycles. In this context, one of the primary components of human milk that is postulated to affect cancer risk is alpha-lactalbumin. Tumour cell death can be induced by HAMLET (a human milk complex of alpha-lactalbumin and oleic acid). HAMLET induces apoptosis only in tumour cells, while normal differentiated cells are resistant to its effects. Therefore, HAMLET may provide safe and effective protection against the development of breast cancer. Mothers should be encouraged to breastfeed their babies because the complex components of human milk secretion make it an ideal food source for babies and clinical evidence has shown that there is a lower risk of breast cancer in women who breastfed their babies.

The present study characterized natural killer cells and cytokines in diabetic mothers, their placenta, and fetus. In the maternal blood from the hyperglycemic groups, the CD16⁺CD56⁻NK cells increased, whereas that of CD16⁺CD56⁺decreased in gestational diabetes mellitus [GDM] group. Cord blood from type 2 diabetes [DM-2] showed a higher proportion of CD16⁺CD56⁻and CD16⁻CD56⁺. The placental extravillous layer of GDM and DM-2 showed an increase of CD16⁺CD56⁻cells and, irrespective of region, the proportion of CD16⁻CD56⁺cells was higher in mild gestational hyperglycemia [MGH] and GDM and lower in DM-2. IL-2 was lower in maternal blood and IFN-γhigher in maternal and cord blood from the GDM group. IL-17 was higher in maternal and cord blood from the DM-2 group. The placental extravillous layer of the MGH showed high levels of IL-4, IL-6, IL-10, IL-17, and IFN-γand low levels of IL-1βand IL-8, whereas the placental villous layer contained high levels of IL-17 and IFN-γ. The GDM group, irrespective of region, showed higher levels of IL-8. The DM-2 group, irrespective of region, placenta showed high levels of TNF-α, IL-17, and IFN-γ. The hyperglycemia produces an inflammatory environment with a high content of inflammatory cytokines and cells expressing CD16⁺.

The adipose tissue has been recognized as an important endocrine organ, which is metabolically active and expresses and secretes various inflammatory cytokines. Inflammation is involved in obesity-related complications. As such, the present study investigated the correlation between biochemical parameters, serum proinflammatory cytokines and adipokines in individuals with obesity. Based on body mass index (BMI), 30 subjects were divided into 3 groups: eutrophic (GC, n = 10), overweight (GOW, n = 10) and obese (GOB, n = 10). Serum glucose, cholesterol (total-C, HDL-C and LDL-C), triglycerides, total proteins, uric acid and insulin were determined, as well as cytokines IL-8, TNF-α, IL-1β, and IL-6, leptin and adiponectin. GOB showed the highest glucose, total and LDL-C, triglycerides, uric acid, insulin, leptin, IL-8, IL-1β, IL-6, TNF-α and adiponectin levels. In general, adiponectin exhibited an inverse correlation with BMI, abdominal circumference, LDL-C, IL-6, TNF-α, leptin and leptin-adiponectin ratio (LAR) and a positive correlation with HDL-C. Leptin was positively correlated with BMI, abdominal circumference, insulin, IL-6, TNF-α and LAR and negatively correlated with HDL-C and adiponectin. The LAR was positively correlated with BMI, waist circumference, insulin, TNF-α and negatively associated with HDL-C. The results confirm that obesity changes the lipid and glycemic profiles of individuals, increases the proinflammatory adipokine levels and reduces those of anti-inflammatory adipokines, promoting a state of chronic inflammation.

Although oxygen, nitrogen, and chlorine reactive species have been associated with disease pathogenesis, their partial absence is very harmful to the body’s innate immune defense. Lacking of adequate release of free radicals from activated phagocytes is related to impaired ability on fungi, bacteria, and protozoa killing. We constructed an updated conceptual landmark regarding the paramount role of free radicals in phagocyte defense systems (phagocyte oxidase, myeloperoxidase, and nitric oxide/peroxynitrite system) on natural immunity. Diverse fungal, bacterial and protozoal pathogens evade the phagocytes’ oxidative/nitrosative burst though antioxidant genes, enzymes and proteins. The most important evasion mechanisms were also described and discussed. These interconnected systems were reviewed and discussed on the basis of knowledge from relevant research groups around the globe. Phagocyte-derived free radicals are essential to destroy important human pathogens during the course of innate immunity.