The intestinal epithelium is a selective barrier where incompletely-digested food antigens are transmitted to the immune system. Food antigens are often the starting point of intestinal diseases such as food allergy or coeliac disease. The intestinal epithelial cells (IEC) take up and process food antigens mainly by fluid-phase transcytosis involving two functional pathways, one minor direct pathway without degradation and another major lysosomal degradative pathway. Among the peptidic metabolites generated during transepithelial transport of luminal antigens, some have a molecular mass compatible with a binding to restriction (major histocompatibility complex; MHC) molecules; the latter can be up regulated on enterocytes, especially in inflammatory conditions. Indeed, interferon-γ not only increases the paracellular absorption of antigens, but also their transcytosis across epithelial cells. It has been reported that enterocytes may even directly present peptidic epitopes to underlying T-cells. As a new potential way of transmitting peptidic information to the local or systemic immune system, the secretion by IEC of antigen-presenting vesicles called exosomes and bearing MHC–peptide complexes has recently been proposed. Many other factors such as nutritional or environmental factors can also influence the properties of the epithelial barrier and the outcome of the immune response to lumen antigens.

In human disease and rodent models, immune responses in the intestinal mucosa can be damaging. Damage is characterised by villus atrophy, crypt hyperplasia and reduced ability to digest and absorb nutrients. In normal individuals active responses to harmless environmental antigens associated with food and commensal bacteria are controlled by the development of immunological tolerance. Similar pathological changes occur in piglets weaned early from their mothers. Active immune responses to food antigens are observed in these piglets, and we and others have hypothesised that the changes occur as a result of transient allergic immune responses to novel food or bacteria antigens. The normal mechanism for producing tolerance to food antigens may operate at induction (Peyer’s patches and mesenteric lymph nodes) or at the effector stage (intestinal lamina propria). In our piglet studies immunological tolerance occurs despite the initial active response. Together with evidence from rodents, this observation suggests that active responses are likely to be controlled at the effector stage, within the intestinal lamina propria. Support for this mechanism comes from the observation that human and pig intestinal T-cells are susceptible to apoptosis, and that this process is accelerated by antigen. We suggest that the role of the normal mature intestinal lamina propria is a balance between immunological effector and regulatory function. In neonatal animals this balance develops slowly and is dependant on contact with antigen. Immunological insults such as weaning may tip the balance of the developing mucosal immune system into excessive effector or regulatory function resulting in transient or chronic allergy or disease susceptibility.

There is good clinical and experimental evidence that oral tolerance exists in man and that the timing of antigen (food) administration is an important factor in the development of food allergic sensitisation and disease. Induction of tolerance is often seen as a T-helper 2-skewed response, which on one side may prevent harmful mucosal immune reactions, but on the other side may contribute to adverse responses in the susceptible individual. The primary mechanisms by which tolerance may be mediated include T-cell deletion, anergy, suppression ‘ignorance’ and apoptosis. Cell-mediated delayed hypersensitivity reactions (T-helper 1), which are implicated as a pathogenetic principle in the development of autoimmune and gastrointestinal inflammation are particularly well suppressed. Regulatory events during the induction of tolerance (or sensitisation) are not well characterised and remain at times controversial. The balance between tolerance (suppression) and sensitisation (priming) is dependent on several factors, such as: (a) genetic background; (b) nature of antigen and dose of antigen; (c) frequency of administration; (d) age (maturity v. immaturity) at first antigen exposure; (e) immunological status of the host (e.g. virus infection); dietary exposure of the mother; (g) antigen transmission via breast milk, and others. Overall, there is evidence in rodents that multiple low-dose feeds are more likely to induce regulatory cytokines (e.g. transforming growth factor-β, interleukins 10 and 4) in part secreted by CD4+CD25+ T-regulatory cells. Despite the powerful suppressive effect of oral antigen exposure observed in experimental models, its application in clinical trials of autoimmune diseases has not yet yielded the expected beneficial results.

The intestinal epithelium acts as a barrier to the external environment contained within the lumen of the gut. It also transports solutes for nutrition and for immunological surveillance. The present review develops the hypothesis that changes in diet, through the composition of the lumen environment, alter the expression of genes in the epithelium. These genes include those that encode for proteins that signal to the mucosal immune system. Directly changing the expression of signalling molecules in the intestinal epithelium using transgenic techniques alters immune function. For example, up regulation of the chemokine macrophage inflammatory protein-2 increases neutrophil recruitment. Furthermore, lumen molecules such as short-chain fatty acids regulate chemokine expression by epithelial cells. By this means, the epithelium acts as a transducing monolayer signalling between the contents of the intestine and the mucosal immune system.

Immunological unresponsiveness or hyporesponsiveness (tolerance) can be induced by feeding protein antigens to naïve animals. Using a classical oral ovalbumin gut-induced tolerance protocol in BALB/c mice we investigated the effects of dietary n-6 and n-3 polyunsaturated fatty acids (PUFA) on high-and low-dose oral tolerance (and in non-tolerised animals, i.e. effects of antigen challenge alone) in relation to lymphoproliferative, cytokine and antibody responses. Fish oil rich in long-chain n-3 fatty acids decreased both T-helper (Th) 1- and Th2-like responses. In contrast, borage (Borago officinalis) oil rich in n-6 PUFA, of which γ-linolenic acid is rapidly metabolised to longer-chain n-6 PUFA, increased Th1-like responses and decreased Th2-like responses, and possibly enhanced suppressor cell or Th3-like activity. These findings are in general agreement with other studies on the effects of long chain n-3 PUFA on immune system functions, and characterise important differences between long-chain n-3 and n-6 PUFA, defining more precisely and broadly the immunological regulatory mechanisms involved. They are also discussed in relation to autoimmune disease.

The provision of food is thought to promote the maintenance of gut integrity. Nutrients are able to elicit and affect both systemic and mucosal immune responses. Enteral diet therapy has long been known to be efficacious in inflammatory bowel disease (IBD), particularly in childhood Crohn's disease. However, the mechanisms of action of these diets are not clear. Nutritional repletion, direct effects on the gut mucosa or decreased intestinal permeability have all been postulated as being important in nutritional therapy. There is some evidence that the enteral diet has a direct effect on the gut mucosa by reducing cytokine production and the accompanying inflammation, thus leading to decreased intestinal permeability. Modifications of enteral diet composition have been evaluated in many studies. Such modifications include fat and/or protein content and the addition of bioactive peptides. The fatty acid composition of the enteral diet seems to have a much greater impact on its efficacy than modification of the N source. As specific fatty acids are precursors of inflammatory mediators derived from arachidonic acid, the reduction in these components may be beneficial in nutritional therapy for IBD. Addition of bioactive peptides to enteral diet formulas may also have a role; such peptides may have specific growth factor or anti-inflammatory actions. There is still much work to be done to define disease-specific enteral diet formulas that are effective as therapies for both Crohn's disease and ulcerative colitis.

Most food-preservation techniques act by slowing down or completely inhibiting the growth of micro-organisms. Few techniques act by inactivating them. While heat remains the technique most extensively used for inactivation, there has been increasing interest recently in the development of alternative approaches in response to the desires of consumers for products which are less organoleptically and nutritionally damaged during processing and less reliant on additives than previously. The new approaches, therefore, mostly involve technologies that offer full or partial alternatives to heat for the inactivation of bacteria, yeasts and moulds. They include the application to foods of high hydrostatic pressure, high-voltage electric discharges, high-intensity laser and non-coherent light pulses, ‘manothermosonication’ (the combination of mild heating with ultrasonication and slightly-raised pressure), and high-magnetic-field pulses. In addition, a number of naturally-occurring antimicrobials, including lysozyme and low-molecular-weight products of micro-organisms are finding increasing use. High pressure is being used commercially to non-thermally pasteurize a number of foods, while the other physical procedures are in various stages of development and commercial evaluation. Possible nutritional consequences have so far been given little attention compared with microbiological ones.

The development of new functional foods requires technologies for incorporating health-promoting ingredients into food without reducing their bioavailability or functionality. In many cases, microencapsulation can provide the necessary protection for these compounds, but in all cases bioavailability should be carefully studied. The present paper gives an overview of the application of various microencapsulation technologies to nutritionally-important compounds, i.e. vitamins, n-3 polyunsaturated fatty acids, Ca, Fe and antioxidants. It also gives a view on future technologies and trends in microencapsulation technology for nutritional applications.

Apart from its main functions of digestion, absorption and faecal processing, the human gastrointestinal tract has a complex pattern of muscular activity regulated by a largely autonomous nervous system, and its various organs contain large concentrations of immune and endocrine tissues. Any failure of these closely-integrated systems can lead to diseases ranging from the mildly irritating to the life threatening. Food contains a huge variety of chemical species, many of which are biologically active, and the distal regions of the gut are colonised by a rich and metabolically-active commensal flora that depend on nutrients derived ultimately from the host’s dietary residues. The present paper explores the evidence for significant effects of food ingredients on functional bowel disorders, intestinal infections, and aspects of epithelial cell physiology involved in the development of colo-rectal neoplasia. Various strategies, including the manipulation of the colo-rectal microflora with pre- and probiotics, and the development of new products and plant varieties containing biologically-active constituents, have the potential to underpin the development of novel functional food products. However, these products will need to be based on proven biological principles, and fully tested for efficacy and safety. The rapidly-developing fields of functional genomics and cell biology will open up new experimental strategies to explore these possibilities, and emerging processing technologies seem likely to provide novel methods for their exploitation.

The present study was funded by the Ministry of Agriculture, Fisheries and Food, its aim being to identify the technical barriers to the development of reduced-fat alternatives for bakery products. Using National Food Survey (Ministry of Agriculture, Fisheries and Food, 1998) statistics on dietary consumption within the home, biscuits, cakes and pastries were identified as contributing significant amounts of fat to the population's dietary intake. Face-to-face interviews were conducted with contacts in the technical community of the baking industry, who were usually working in technical and new-product development functions. A discussion guide was developed to cover the main lines of enquiry. The companies selected were ingredient suppliers (eight), manufacturers (twelve) and retailers (four) and so represented each step of the food supply chain. In brief, results showed that current labelling rules were too stringent, and constrained development of reduced-fat bakery products. Products with lower fat levels are harder to make due to altered handling and processing properties. Their quality is usually poorer than standard products, particularly for flavour, texture and mouthfeel. The perception of freshness is reduced and product shelf-life may consequently be shorter. For the product developer, there are relatively few ingredients that can be used in place of fat, and knowledge of how they work is limited, which inhibits product development. There is no identifiable source of technical knowledge in this field. Consumers perceive reduced-fat bakery products to be of lower quality and are generally unwilling to pay higher prices than for standard products.

It is thought that nutrition during pregnancy plays a key role in the well-being of the mother and the newborn infant, and further influences health during childhood and adulthood. Pregnancy is a time of increased nutritional requirements, but many of these requirements will be met by adaptive physiological changes that occur during gestation, with little need to alter maternal dietary intake. A modest increment of food which provides 0.8 MJ/d (above prepregnant requirements) during the third trimester is considered adequate to meet the needs of fetal and maternal growth, and to satisfy the small increase in requirements of many macro- and micronutrients. However, requirements for vitamin D and folic acid increase substantially, and should be met primarily by supplementation. Food selection may also be altered to avoid a range of food-borne diseases and toxic constituents. There are a number of psycho-social reasons why pregnancy might be considered a good time for promoting changes in dietary behaviour for the health of the wider family. However, pregnancy may be a bad time to promote dietary change if it is perceived to involve slimming, if nutritional requirements are greatest before pregnancy, or if dietary changes made are harmful. There is little evidence to support educational interventions as successful at changing dietary behaviour during pregnancy. Pregnancy may be best viewed as an opportunity for maintaining good dietary selections and for building knowledge for future action, and should not be seen as the only opportunity for promoting dietary change within the life course.

A substantial and robust body of epidemiological evidence indicates that prenatal dietary experience may be a factor determining cardiovascular disease risk. Retrospective cohort studies indicate that low birth weight and disproportion at birth are powerful predictors of later disease risk. This prenatal influence on non-communicable disease in later life has been termed programming. Maternal nutritional status has been proposed to be the major programming influence on the developing fetus. The evidence from epidemiological studies of nutrition, fetal development and birth outcome is, however, often weak and inconclusive. The validity of the nutritional programming concept is highly dependent on experimental studies in animals. The feeding of low-protein diets in rat pregnancy results in perturbations in fetal growth and dimensions at birth. The offspring of rats fed low-protein diets exhibit a number of metabolic and physiological disturbances, and are consistently found to have high blood pressure from early postnatal life. This experimental model has been used to explore potential mechanisms of programming through which maternal diet may programme the cardiovascular function of the fetus. Indications from this work are that fetal exposure to maternally-derived glucocorticoids plays a key role in the programming mechanism. Secondary to this activity, the fetal hypothalamic–pituitary–adrenal axis may stimulate renin–angiotensin system activity, resulting in increased vascular resistance and hypertension.

The physiological processes that underlie the reproductive cycle impose considerable metabolisable protein (MP) demands on a female, especially during the periparturient period. When MP supply falls short of MP demand (i.e. MP becomes scarce), certain, if not all, bodily functions are expected to be penalised. It has been proposed that partitioning of scarce MP is prioritised to reproductive rather than to immune functions. In other words, at times of MP scarcity, the penalty on expression of immunity would be expected to be greater than that on reproduction. This hypothesis forms a nutritional basis for the occurrence of periparturient breakdown of immunity to parasites (BIP), which can be observed in many host–parasite systems. In the present review we explore this nutritional basis, using periparturient sheep infected with the abomasal nematode Teladorsagia circumcincta as an example, and attempt to quantify its occurrence. Evidence supporting the nutritional basis of periparturient BIP is reviewed, covering experiments in which nutrient supply (from both exogenous and endogenous sources) and/or nutrient demand were manipulated. Quantitatively, MP requirements for expression of immunity to T. circumcincta were estimated to be about 1 g/kg metabolic body weight (body weight0·75) per d, approximately 5 % of the maximum MP requirements of periparturient sheep. The major component of this requirement was assumed to be for replenishing irreversible plasma protein losses into the gastrointestinal tract. Although confirmation of this estimate is required, such estimates may be used to improve the known MP requirements of periparturient animals, enabling the extent and the consequences of periparturient BIP to be minimised.

The modern dairy cow has been selectively bred to produce large amounts of milk. Partly as a result, food consumption is considerably less than milk energy output in early lactation. It is only at 2 months or more postpartum that intake increases to the point where positive energy balance is regained, the initial production being achieved by a substantial mobilisation of body reserves. These reserves are laid down before parturition, but it is certainly not the case that the pregnant cow will accumulate adipose tissue recklessly; in the last third of pregnancy well-fed cows in good body condition exhibit reduced, not increased, appetite. There is a fine balancing act to perform. Excessive body condition at parturition quickly leads to metabolic problems such as ketosis, but cows who subsequently become too thin have increased risk of metabolic diseases such as mastitis and lameness. The biological mechanisms regulating output of milk are reasonably well understood, those controlling appetite less well so, and there has been little attempt at systematic integration of the two. The transition from pregnancy to lactation represents a major challenge to homeostasis, made more complicated in multiparous cows by the fact that much of gestation is concurrent with lactation. Herein lies the potential for nutritionally-entrained flexibility. In the wild, concurrent pregnancy and lactation only occur when nutritional conditions are favourable. If conditions are poor, rebreeding will be delayed and lactation will continue, at an energetically-sustainable level, for much longer than its ‘normal’ duration. In this way the twin energetic burdens of pregnancy and lactation are separated, and extremes are avoided. Given the increasing public concern about stresses suffered by intensively-managed dairy cows, this case may be one where commercial dairying could learn useful lessons from nature.