Background: Several elements in colostrum and human milk, including antibodies and nonspecific factors with bactericidal and antiviral activity, may play an important anti-infectious and protective role. In developing countries, enterotoxigenic Escherichia coli (ETEC) is the main etiological agent of diarrhea in low-socioeconomic level children. In the present work, we studied the functional activity of mononuclear (MN) and polymorphonuclear (PMN) phagocytes of human colostrum against ETEC, as well as the interactions between these cells and colostral or serum opsonins. Methods: Colostrum samples were collected from 33 clinically healthy women between 48 and 72 hours postpartum. We verified superoxide release in colostral MN and PMN using cytochrome C reduction methods, phagocytosis, and bactericidal activity using acridine orange methods and superoxide dismutase (SOD) in the colostrum supernatants. Results: Colostral MN and PMN phagocytes exposed to ETEC opsonized with colostrum supernatants caused a significant increase (p< 0.05) in superoxide release. Phagocytosis by colostral PMN cells increased significantly (p< 0.5) when the phagocytes were incubated with both sources of opsonins (sera and colostrum). Increases in superoxide release in the presence of opsonized bacteria triggered the bactericidal activity of the phagocytes. Phagocyte treatment with SOD decreased their ability to eliminate ETEC. Colostrum supernatant had higher SOD concentrations (p< 0.05) compared with normal human sera. Conclusions: 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. © 2011.
França, E. L., Bitencourt, R. V., Fujimori, M., Cristina de Morais, T., de Mattos Paranhos Calderon, I., & Honorio-França, A. C. (2011). Human colostral phagocytes eliminate enterotoxigenic Escherichia coli opsonized by colostrum supernatant. Journal of Microbiology, Immunology and Infection, 44(1), 1–7. https://doi.org/10.1016/j.jmii.2011.01.002