Honorio-França AC, Carvalho MPSM, Isaac L, Trabulsi LR, Carneiro-Sampaio MMS. Colostral Mononuclear Phagocytes are Able to Kill Enteropathogenic Escherichia coli Opsonized with Colostral IgA. Scand J Immunol 1997;46:59-66 Enteropathogenic Escherichia coli (EPEC) is the main aetiological agent of acute diarrhoea among low socioeconomic level infants in developing countries. Breast-feeding provides infant protection against acute gastrointestinal and respiratory infections; however, little is known about the protective role of colostral phagocytes in the gut of newborn infants. In the present investigation we studied the ability of human colostral MN phagocytes to kill EPEC as well as the interactions between these cells and colostral and serum opsonins. The authors observed that the microbicidal activity of colostrum MN phagocytes was dependent on previous EPEC opsonization with colostral supernatant or blood serum. A defatted colostrum supernatant pool presented opsonic activity for EPEC killing at levels equivalent to those of normal serum. IgA-depleted colostrum supernatant showed significantly lower opsonic activity, whereas purified IgA from the same colostrum pool was a potent opsonin which induced EPEC killing at levels equivalent to those of untreated colostrum. Colostral MN phagocytes are able to release superoxide anion when incubated with both EPEC opsonized with untreated colostrum and purified IgA. Purified IgA was also able to restore opsonic activity of IgA-depleted colostrum. A colostrum pool without C3 and IgG induced EPEC killing by colostral MN phagocytes at rates equivalent to those of untreated colostrum supernatant. Addition of an IgM MoAb (My43) anti-human Fca receptor resulted in a significant inhibition of EPEC killing when bacteria were opsonized with purified IgA, suggesting an interaction between IgA and FcaR. With respect to serum opsonins, we observed that IgG plus complement component C3 were necessary to induce EPEC killing by the colostrum MN phagocytes. Colostral phagocyte killing of enteropathogenic bacteria may represent an additional mechanism of breast-feeding protein against intestinal infections during the first week of life.

These results suggest that the ability of phagocytes to eliminate ETEC depends on the activation of cellular oxidative metabolism; moreover, activation of colostral phagocytes is likely an additional breast-feeding protection mechanism against intestinal infections in infants.

BackgroundObesity 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.MethodsColostrum 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).ResultsGlucose 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.ConclusionsThe 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.

Some studies report that hormone melatonin can be found in human milk, but the daily variation in colostrummelatonin is not available. This study verified the effects of milk collection time (diurnal/nocturnal) on colostralmelatonin levels and the ability of this hormone to modulate colostral phagocyte activity. Colostrum sampleswere collected from 30 mothers during the day and night, for a total of 60 samples. We determined melatoninlevels in colostrum and superoxide release and bacterial killing by colostral phagocytes. Melatonin levelswere higher in colostrum samples collected at night. Phagocytes in nocturnal colostrum samples increasedspontaneous superoxide release. In diurnal colostrum samples, mononuclear (MN) phagocytes increasedsuperoxide release when exposed to enteropathogenic Escherichia coli (EPEC), but not polymorphonuclear(PMN) phagocytes. Phagocytes exposed to both EPEC and melatonin had higher superoxide release,independent of phagocyte type and colostrum collection period. Phagocytosis rate was higher in colostrumsamples collected at night. In diurnal samples, EPEC killing by MN phagocytes was lower than by PMNphagocytes. Phagocytosis increased significantly in the presence of melatonin in both MN and PMN cells,irrespective of colostrum collection period. In response to melatonin, MN phagocytes from both diurnaland nocturnal samples increased bactericidal activity, whereas colostral PMN phagocytes increased it onlyin diurnal samples. The melatonin increased in the intracellular Ca2+ levels. The highest intracellular Ca2+release were found in MN phagocytes diurnal samples. These results confirm that melatonin levels in humancolostrum follow a day-night variation and increase phagocytic activity of colostral cells against bacteria