At birth, when immune responses are insufficient, there begins the development of the defence capability against pathogens. Leptin and adiponectin, adipokines that are present in breast milk, have been shown to play a role in the regulation of immune responses. We report here, for the first time, the influence of in vivo adipokine supplementation on the intestinal immune system in early life. Suckling Wistar rats were daily supplemented with leptin (0·7 μg/kg per d, n 36) or adiponectin (35 μg/kg per d, n 36) during the suckling period. The lymphocyte composition, proliferation and cytokine secretion from mesenteric lymph node lymphocytes (on days 14 and 21), as well as intestinal IgA and IgM concentration (day 21), were evaluated. At day 14, leptin supplementation significantly increased the TCRαβ+ cell proportion in mesenteric lymph nodes, in particular owing to an increase in the TCRαβ+ CD8+ cell population. Moreover, the leptin or adiponectin supplementation promoted the early development CD8+ cells, with adiponectin being the only adipokine capable of enhancing the lymphoproliferative ability at the end of the suckling period. Although leptin decreased intestinal IgA concentration, it had a trophic effect on the intestine in early life. Supplementation of both adipokines modulated the cytokine profile during (day 14) and at the end (day 21) of the suckling period. These results suggest that leptin and adiponectin during suckling play a role in the development of mucosal immunity in early life.

The present study investigated the effect of feeding bovine colostrum (BC) to piglets in comparison with feeding a milk replacer (MR) and conventional rearing by the sow on the intestinal immune system and number of enterotoxigenic Escherichia coli (ETEC) colonising the intestinal tissue. Piglets (23-d-old) were allocated to one of the following four groups: (1) killed at the beginning of the experiment (Base); (2) separated from the sow and fed BC (BC-fed); (3) separated from the sow and fed a MR (MR-fed); (4) kept with the sow (Sow-Milk). Blood was sampled on days 1 and 8, and faecal samples were collected on days 1, 3, 5 and 8. On day 8, piglets were killed and gastrointestinal digesta and intestinal segments were collected. The frequency of diarrhoea was found to be higher (P≤ 0·019) in MR-fed piglets than in BC-fed and Sow-Milk piglets. Piglets from the MR-fed group had the lowest lactic acid bacteria:haemolytic E. coli ratio (P treat= 0·064) in the faeces. The number of E. coli colonising the intestinal tissue was higher (P< 0·001) in piglets from the MR-fed group than in those from the BC-fed and Sow-Milk groups. Piglets from the Sow-Milk group had a higher (P= 0·020) mucosal IgG concentration than those from the MR-fed group, but did not exhibit any difference when compared with piglets from the Base and BC-fed groups. Piglets from the BC-fed group exhibited a reduced (P≤ 0·037) expression level of Toll-like receptor-4 in the intestinal mucosa when compared with those from the MR-fed and Sow-Milk groups. The expression level of IL-2 was higher (P≤ 0·051) in piglets from the MR-fed group than in those from the other treatment groups. In conclusion, feeding BC rather than MR to the piglets reduced the colonisation of intestine by ETEC and modulated the intestinal immune system, whereas no differences were observed in piglets fed BC and conventionally reared by the sows.

The present study was conducted to test the hypothesis that low concentrations of coated ZnO, as a substitute for a high concentration of ZnO (2250 mg Zn/kg), could improve intestinal immunity function and regulate microbiota composition, thus alleviating the incidence of diarrhoea in weaned piglets. A total of eighty-four cross-bred piglets, weaned at an age of 28 (sem 1) d, were allocated randomly, on the basis of average initial body weight (7·72 (sem 0·65) kg), to seven treatment groups as follows: a 250 mg Zn (ZnO)/kg group (low Zn; LZ) and a 2250 mg Zn (ZnO)/kg group (high Zn; HZ) that were offered diets containing ZnO at 250 and 2250 mg Zn/kg, respectively; and five experimental groups in which coated ZnO was added at 250, 380, 570, 760 and 1140 mg Zn/kg basal diet, respectively. The trial lasted 2 weeks. The results indicated that, compared with LZ treatment, supplementation with coated ZnO at 380 or 570 mg Zn/kg reduced (P< 0·05) diarrhoea index, increased (P< 0·05) duodenal villus height and the ratio of villus height:crypt depth, up-regulated (P< 0·05) the gene expression of insulin-like growth factor 1, zonula occludens protein-1, occludin, IL-10 and transforming growth factor β1, and elevated (P< 0·05) secretory IgA concentration in the jejunal mucosa. Microbiota richness and the Shannon diversity index were also decreased (P< 0·05). Furthermore, piglets in the group fed coated ZnO at 380 or 570 mg Zn/kg did not differ from those in the HZ-fed group in relation to the aforementioned parameters. Collectively, a low concentration of coated ZnO (380 or 570 mg Zn/kg) can alleviate the incidence of diarrhoea by promoting intestinal development, protecting the intestinal mucosal barrier from damage, stimulating the mucosal immune system and regulating the microbiota composition.

Analyses of laboratory-based helminth-rodent model systems have been immensely useful in delineating the workings of the mammalian immune system. Investigations in the 1970s–1980s on the fate of the rat tapeworm, Hymenolepis diminuta, in rats and mice and the systemic and local responses evoked following infection have contributed directly to our knowledge of how permissive and non-permissive hosts respond to the challenge of infection with a helminth parasite. This convenient laboratory model system has, in the authors' opinion, regrettably received considerably less attention in recent years. With the goal of highlighting the utility of this model system, data is presented on: (1) the immune and enteric responses of rats and mice to infection with H. diminuta; (2) the ability of excretory or secretory products derived from H. diminuta to significantly reduce T cell and macrophage activation in vitro; and (3) how assessment of H. diminuta-rodent models can be used to identify immune effector or regulatory mechanisms that can be translated into novel treatments for inflammatory and autoimmune disorders.

Experiments were carried out to explore the survival of 14-day adult H. polygyrus following transplantation to mice of four strains, immunized by various protocols. Adult worm establishment and survival was unimpaired in CFLP mice which were totally refractory to larval challenge. Transplanted adult worms were also successful in NIH mice immunized by the 9-day abbreviated infection regime. However, NIH mice exposed to irradiated larvae or subjected to the divided primary infection, expelled transplanted adults. The 9-day abbreviated infection was further examined in SJL and (C57 Bl10 X NIH) F1 mice which expel adult worms during a primary infection and although this regime was unsuccessful in causing NIH mice to reject adult worms, expulsion of adult worms was accelerated in SJL and F1 mice. The survival of adult H. polygyrus was discussed in the context of stage-specific immunity and the delicate balance between the immunogenic stimuli from developing larvae, the immunomodulatory activities of adult stages and the host's genetically determined capacity to respond to these opposing signals.

The therapeutic and preventive effects of yogurt and lactic acid bacteria on diseases such as cancer, infection and gastrointestinal disorders are well documented. The aim of this research was to study the effects of different doses of yogurt addition after milk re-nutrition diet, on the recovery of the intestinal barrier and mucosal immune function. Experiments were performed on groups of mice, malnourished and re-nourished with milk during 7 d, and mice with diet supplemented with yogurt for 2, 5 and 7 consecutive d. Nutritional parameters such as weight gain, serum total protein, and the number of IgA, IgM and IgG B cells of the small intestine were determined. We also quantified intraepithelial leukocytes, mastocytes and goblet cells, and performed structural and ultrastructural studies on the small intestine. We observed that 5 d of yogurt feeding was the optimal dose for improving gut barrier function and mucosal immune system in a malnutrition model. This effect was not observed with milk re-nutrition. Although the results were better for 5 d of yogurt, addition for 7 d also showed beneficial effects. Yogurt feeding in our model did not impair any gut functions. These results suggest that yogurt addition after a re-nutrition diet gives better recovery of intestinal function than the re-nutrition diet usually recommended. Although these results were obtained in an animal model, they indicate that consumption of yogurt by malnourished children might accelerate the restoration of gut function.