There have been considerable advances in our understanding of the diverse mixture of bioactive components in human milk that influence the immune status of infants by not only providing protection but also facilitating development, tolerance, and an appropriate inflammatory response. It could be suggested that milk is the communication vehicle between the maternal immune system and the infant, a system actively directing and educating the immune, metabolic, and microflora systems within the infant, while conferring multiple means of protection from pathogens. The physiological and protective functions of many of the immune components in human milk have been deduced not from studies in infants but from what is known in other species and in vitro models. This update briefly reviews immune development in infants and focuses on current knowledge of how both the "classical" immune and the nonimmune ingredients found in mature human milk promote immune development, facilitate the development of tolerance, and regulate the inflammatory response of infants.

The gastrointestinal tract is subjected to enormous and continual foreign antigenic stimuli from food and microbes. This organ must integrate complex interactions among diet, external pathogens, and local immunological and non-immunological processes. It is critical that protective immune responses are made to potential pathogens, while hypersensitivity reactions to dietary antigens are minimised. There is increasing evidence that fermentable dietary fibres and the newly described prebiotics can modulate various properties of the immune system, including those of the gut-associated lymphoid tissues (GALT). This paper reviews evidence for the immune-enhancing effects of dietary fibres. Changes in the intestinal microflora that occur with the consumption of prebiotic fibres may potentially mediate immune changes via: the direct contact of lactic acid bacteria or bacterial products (cell wall or cytoplasmic components) with immune cells in the intestine; the production of short-chain fatty acids from fibre fermentation; or by changes in mucin production. Although further work is needed to better define the changes, mechanisms for immunomodulation, and the ultimate impact on immune health, there is convincing preliminary data to suggest that the consumption of prebiotics can modulate immune parameters in GALT, secondary lymphoid tissues and peripheral circulation. Future protocols on the physiological impact of consuming prebiotics should be designed to include assessments of the gut microflora, gut physiology and the function and composition of the various regions of GALT.

To determine the mechanism by which the (n-3) fatty acids (FA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decrease proliferation and induce apoptosis in MDA-MB-231 human breast cancer cells, we examined the effects of EPA and DHA on the lipid composition of lipid rafts as well as epidermal growth factor receptor (EGFR) raft localization and phosphorylation. (n-3) FA (a combination of EPA and DHA) inhibited (P < 0.05) the growth of MDA-MB-231 cells by 48-62% in the presence and absence, respectively, of linoleic acid (LA). More EPA and DHA were incorporated into lipid rafts isolated from MDA-MB-231 cells after treatment with (n-3) FA compared with cells treated with LA (P < 0.05). EPA and DHA treatment decreased (P < 0.05) lipid raft sphingomyelin, cholesterol, and diacylglycerol content and, in the absence of LA, EPA and DHA increased (P < 0.05) raft ceramide levels. Furthermore, there was a marked decrease in EGFR levels in lipid rafts, accompanied by increases in the phosphorylation of both EGFR and p38 mitogen-activated protein kinase (MAPK), in EPA+DHA-treated cells (P < 0.05). As sustained activation of the EGFR and p38 MAPK has been associated with apoptosis in human breast cancer cells, our results indicate that (n-3) FA modify the lipid composition of membrane rafts and alter EGFR signaling in a way that decreases the growth of breast tumors.

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Ileal proglucagon gene expression and postprandial plasma concentrations of proglucagon-derived peptides are reported to change with the type and quantity of dietary fiber ingested by rats. Within the intestine, proglucagon encodes several proglucagon-derived peptides known to modulate intestinal absorption capacity and pancreatic insulin secretion. To determine whether the chronic ingestion of fermentable dietary fiber regulates the expression and synthesis of proglucagon-derived peptides in the distal intestine to modulate glucose homeostasis, the following study was conducted: 16 adult dogs (23 +/- 2 kg) were fed isoenergetic, isonitrogenous diets containing a mixture of high fermentable dietary fibers (HFF) or low fermentable (LFF) wood cellulose for 14 d in a randomized cross-over design. Food was withheld for 16 h before an oral glucose tolerance test was conducted supplying 2 g of glucose/kg body wt, and peripheral blood was collected via a hind-leg catheter at 0, 15, 30, 45, 60, 90 and 120 min for plasma glucose, insulin and glucagon-like peptide-1(7-36)NH2 (GLP-1) analyses. Intestinal samples were collected after the second dietary treatment. Ileal proglucagon mRNA, intestinal (GLP-1) concentrations and the integrated area under the curves (AUC) for plasma GLP-1 and insulin were greater and plasma glucose AUC was reduced when dogs were fed the HFF diet compared to the LFF diet (P < 0.05). Intestinal villi heights, brush border and basolateral glucose transporter protein abundance and jejunal transport capacities were significantly greater when dogs were fed the HFF diet than when fed the LFF diet. In conclusion, improvements in glucose homeostasis are observed in healthy dogs when they ingest fermentable fibers.