Inhibition of enterotoxigenic Escherichia coli (ETEC) adhesion to Caco-2 cells by human milk and its immunoglobulin and non-immunoglobulin fractions

Abstract

Enterotoxigenic Escherichia coli (ETEC) is the most common cause of diarrhea in children in developing countries and among travelers to ETEC endemic areas. ETEC diarrhea is caused by colonization of the small intestine mediated by colonization factor (CF) antigens, and subsequent elaboration of enterotoxins. Breast feeding has been related to protection against enteric infections. The protective effect of human milk can be ascribed to its immunoglobulin content, specially secretory immunoglobulin A (sIgA), and to nonimmunoglobulin components such as free oligosaccharides, glycoproteins and glycolipids. In this study we investigated the effect of whole human milk and its fractions immunoglobulin and non-immunoglobulin on the adherence of ETEC strains possessing different CFs to Caco-2 cells, as well as the ability of sIgA and free secretory component (fSC) to bind to bacterial superficial proteins. Pooled human milk from three donors were fractionated by gel filtration and analyzed by SDS-PAGE. Our results revealed that whole human milk and its proteins fractions, containing sIgA and fSC, inhibited adhesion ETEC strains harboring different colonization factors antigens. We also verified that sIgA and fSC, using immunoblotting and immunogold labeling assays, bound to some fimbrial proteins and other material present in bacterial surface. Our findings suggest that whole human milk and its fractions may contribute to protection against ETEC infections by blocking bacterial adhesion mediated by different colonization antigens.

Human colostral phagocytes eliminate enterotoxigenic Escherichia coli opsonized by colostrum supernatant

“…The functional activity of phagocytes described in this work reinforces the findings of other studies that demonstrate the importance of breastfeeding in combating these enterobacteriaceae. 8,43 ETEC diarrhea affects mainly children under the age of 2 years, and its incidence decreases over time. 44 The ability of phagocytes to eliminate ETEC depends on the activation of cellular oxidative metabolism; in addition, activation of colostral phagocytes is likely an additional breast-feeding protection mechanism for infants against intestinal infections and may represent an important source of protection against infections during this phase of life and may persist until maturity of the infant's immune system is well developed.…”

“…19 Human milk contains antibodies against a variety of bacteria, and colostrum inhibits the adhesion of different ETEC serotypes. 8 Components other than immunoglobulins (i.e. oligosaccharides, glycoproteins, and glycolipids) also seem to prevent the adhesion of ETEC strains to host cells.…”

“…oligosaccharides, glycoproteins, and glycolipids) also seem to prevent the adhesion of ETEC strains to host cells. 8 Phagocytes in human colostrum possibly act in conjunction with soluble components, thereby providing an additional protection mechanism against enterobacterial infection. However, studies on the functional activity of colostral MN and PMN phagocytes and their interactions with the bioactive components of colostrum are only partially understood.…”

Bioactive Immune Components of Anti-Diarrheagenic Enterotoxigenic Escherichia coli Hyperimmune Bovine Colostrum Products

“…The comparable results obtained for IMM-124E powder and tablets in every test performed confirmed the preservation of active ingredients in the final product. The HBC preparations contained lactoferrin, a potent antimicrobial protein capable of inhibiting ETEC growth and adherence to epithelial cells in vitro ( 29 , 30 ). Interestingly, higher levels of lactoferrin were found in ProMilk than in the HBC powders and tablets, possibly reflecting the concentrated proteins contained in this product.…”

Bovine Lactoferrin Decreases Cholera-Toxin-Induced Intestinal Fluid Accumulation in Mice by Ganglioside Interaction

“…Lactoferrin has a bactericidal effect on ETEC strains isolated from pigs in vitro [21]. Binding of lactoferrin to E. coli colonization factors [22] causes inhibition of hemagglutination [23] and inhibition of adherence of ETEC to epithelial cells in vitro [24] and to intestinal mucosa of germfree mice in vivo [25]. Therefore, we speculated that bLF might exhibit the anti-diarrheal ability by both the suppression of intestinal bacterial growth and the blocking of binding of toxin to cellular receptor.…”