Intestinal microbiota may influence human physiology and disease risk due to the role it plays in mediating appropriate immune responses to harmful and innocuous antigens. Colonisation of the intestine in early life seems particularly important as it is the main environmental stimulus for immune system maturation. This is a dynamic process, which depends on both environmental and genetic factors. The pathogenesis of inflammatory bowel disease, such as Crohn's disease, involves genetic polymorphisms (e.g. CARD15/nucleotide-binding oligomerisation domain 2) related to an excessive inflammatory response to commensal microbiota and to its unbalanced composition. Atopic diseases have also been linked to imbalances in microbiota and to related genetic factors (e.g. TLR4 and CD14 genes), although these associations are still controversial. Research into the relationship between the genetic risk of developing celiac disease (human leukocyte antigen (HLA)-DQ2/DQ8) and the early colonisation process in infants at family risk of the disease has also reported that the HLA-DQ genotype could influence staphylococcal colonisation. Future observational studies considering both host genetics and microbiota could be critical in defining the complex host–microbe interactions and the respective role each plays in inflammatory disorders.

Recently, there has been much interest in the literature in the role of early nutrition and the health of the individual in adulthood. A majority of infants in the UK are born full term, while preterm infants account for 4–6 % of the total births. Milk feeding practices are divided into three groups: breast, combination (breast-fed with formula as‘top-up) and bottle (formula). In studies conducted by our group and other researchers immune function in full-term and preterm infants has been assessed by monitoring total and specific immunoglobulin E and specific immunoglobulin G levels. Dietary modification by the pregnant mother with a history of allergy in the family has been shown to have a positive effect with respect to allergy outcome and prevention of atopic disease in the infant. However, this dietary modification has to occur before week 22 of pregnancy and continue until the end of lactation to achieve a beneficial outcome to the infant. The stress of mothers restricting their diets may be disadvantageous to the fetus, and therefore any gain due to the dietary restriction may be lost. Researchers have shown that the early introduction of complementary foods and the greater diversity of these foods appeared to result in an increase in the incidence of atopic disease in the infant. In conclusion, in order to reduce the risk in their babies, mothers with a family history of atopic disease should breast-feed for more than 15 weeks and introduce solid foods after 4 months, limiting the variety until at least 6 months.

The aim of this study was to assess the impact of dietary counselling combined with the provision of food products on food and nutrient intake in pregnant women. We carried out a prospective cohort study of healthy and atopic pregnant women (n 209), who were randomized into dietary intervention and control groups. The intervention group received dietary counselling and food products to modify the fat composition of their diet to meet current recommendations. Three-day food records were collected during each trimester of pregnancy. Women in the intervention group consumed more vegetables, fruits, soft margarines and vegetable oils and less butter than those in the control group during the course of pregnancy (P < 0·05). The main distinction between the groups in nutrient intake over the pregnancy was attributable to a higher energy intake (% energy) of PUFA by 0·5 %energy (95 % CI 0·1, 0·8) and to a lower intake of SFA by 0·8 % energy (95 % CI − 1·4, − 0·4) in the intervention group. Dietary intake of vitamin E was 1·4 mg (95 % CI 0·6, 2·2), folate 20·9 μg (95 % CI 0·8, 41·0) and ascorbic acid 19·8 mg (95 % CI 3·5, 36·0) higher in the intervention group compared to the controls, while no differences in other nutrients were detected. Dietary counselling combined with the provision of food products during pregnancy is of importance in modifying food and nutrient intake, with potential health benefits.

The immune system exists to protect the host against pathogenic organisms and highly complex pathways of recognition, response, elimination and memory have evolved in order to fulfil this role. The immune system also acts to ensure tolerance to ‘self’, to food and other environmental components, and to commensal bacteria. A breakdown in the tolerogenic pathways can also lead to inflammatory diseases. The prevalence of inflammatory diseases, including atopic disorders, has increased over the last 60 years. The development of tolerance is the result of active immune mechanisms and both development and maintenance of tolerance are lifelong processes which start very early in life, even prenatally. Profound immunologic changes occur during pregnancy, involving a polarization of T helper (Th) cells towards a dominance of Th2 and regulatory T cell effector responses in both mother and fetus. This situation is important to maintain pregnancy through avoidance of the rejection of the immunologically incompatible fetus. During the third trimester of human pregnancy, fetal T cells are able to mount antigen-specific responses to environmental and food-derived antigens and antigen-specific T cells are detectable in cord blood in virtually all newborns indicating in utero sensitization. If the neonatal immune system is not able to down-regulate the pre-existing Th2 dominance effectively then an allergic phenotype may develop. Changes occur at, and soon after, birth in order that the immune system of the neonate becomes competent and functional and that the gut becomes colonized with bacteria. Exposure to bacteria during birth and from the mother's skin and the provision of immunologic factors in breast milk are amongst the key events that promote maturation of the infant's gut and gut-associated and systemic immune systems. The introduction of formula and of solid foods exposes the infant to novel food antigens and also affects the gut flora. Nutrition may be the source of antigens to which the immune system must become tolerant, provide factors, including nutrients, that themselves might modulate immune maturation and responses, and provide factors that influence intestinal flora, which in turn will affect antigen exposure, immune maturation and immune responses. Through these mechanisms it is possible that nutrition early in life might affect later immune competence, the ability to mount an appropriate immune response upon infection, the ability to develop a tolerogenic response to ‘self’ and to benign environmental antigens, and the development of immunologic disorders. A Workshop held in February 2006 considered recent findings in the areas of oral tolerance, routes of sensitization to allergens and factors affecting the development of atopic disease; factors influencing the maturation of dendritic cells and the development of regulatory T cells; the influence of gut microflora on immunity, allergic sensitization and infectious disease; the role of nutrition in preventing necrotizing enterocolitis in an animal model of preterm birth; and the role of PUFA of different classes in influencing immune responses and in shaping the development of atopic disease. This report summarizes the content of the lectures and the subsequent discussions.

The challenge for the modern health care system is to fight against the increasing prevalence of atopic disease. The introduction of scientifically composed probiotic functional foods for prophylactic or therapeutic purposes could be one solution. Probiotics are live microbial food supplements or components of bacteria which have beneficial effects on human health. Specific strains have been demonstrated to exert powerful anti-pathogenic, anti-inflammatory and anti-allergic effects. The hygiene hypothesis suggests that atopic disease may arise from a lack of counterbalancing microbial exposure at an early age. The initial compositional development of the gut microflora is considered a key determinant of the development of both the immune responder phenotype and normal gut barrier functions. The regulatory role of probiotics in human allergic disease was first emphasised in the demonstration of a suppressive effect on lymphocyte proliferation and interleukin-4 generation in vitro. Subsequently, a significant improvement in the clinical course of atopic eczema was reported in infants given a probiotic-supplemented diet. The potential of probiotics to reduce the risk of atopic disease has recently been demonstrated in a double-blind, placebo-controlled study: probiotics administered pre- and postnatally for 6 months to at-risk subjects reduced the prevalence of atopic eczema to half of that observed in infants receiving placebo. Ongoing research is directed towards the development of novel techniques to characterise the gut microflora. Future research will clarify the mechanisms to control specific physiological processes in the evolution of atopic disease in at-risk populations or in the management of allergic diseases.