Obestatin is a gastrointestinal peptide having wide-ranging effects on cell proliferation; however, its mechanism of action remains poorly understood. Thus, the aim of the study was to elucidate the effect of exogenous obestatin on the postnatal structural development of the small intestine. Seven-day-old piglets with an average BW of 1.56 ± 0.23 kg were divided into four groups (n = 10) that received intragastrically obestatin (2, 10 or 15 μg/kg BW) or vehicle. After a 6-day experimental period, morphological analysis of gastrointestinal tract and small intestine wall (mitosis and apoptosis indexes, histomorphometry of mucosa and muscularis layers) was performed. The study revealed a seemingly incoherent pattern of the histological structure of the small intestine among the experimental groups, suggesting that the effect of obestatin is both intestinal segment specific and dose dependent. Histomorphometric analysis of the small intestine showed that higher doses of obestatin seem to promote the structural development of the duodenum while simultaneously hindering the maturation of more distal parts of the intestine. Intragastric administration of obestatin increased the crypt mitotic index in all segments of the small intestine with the strongest pro-mitotic activity following the administration of obestatin at a dose of 10 and 15 μg/kg BW. The significant differences in the number of apoptotic cells in the intestinal villi among the groups were observed only in proximal jejunum and ileum. In conclusion, it seems that obestatin shows a broad-spectrum of activity in the gastrointestinal tract of newborn piglets, being able to accelerate its structural development. However, the varied effect depending on the intestinal segment or the concentration of exogenous obestatin causes that further research is needed to clarify the exact mechanism of this phenomenon.

Ca plays an essential role in bone development; however, little is known about its effect on intestinal gene expression in juvenile animals. In the present study, thirty-two weaned pigs (9·5 (sem 0·11) kg) were assigned to four diets that differed in Ca concentration (adequate v. high) and cereal composition (wheat–barley v. maize) to assess the jejunal and colonic gene expression of nutrient transporters, tight junction proteins, cytokines and pathogen-associated molecular patterns, nutrient digestibility, Ca balance and serum acute-phase response. To estimate the impact of mucosal bacteria on colonic gene expression, Spearman's correlations between colonic gene expression and bacterial abundance were computed. Faecal Ca excretion indicated that more Ca was available along the intestinal tract of the pigs fed high Ca diets as compared to the pigs fed adequate Ca diets (P< 0·05). High Ca diets decreased jejunal zonula occludens 1 (ZO1) and occludin (OCLN) expression, up-regulated jejunal expression of toll-like receptor 2 (TLR2) and down-regulated colonic GLUT2 expression as compared to the adequate Ca diets (P< 0·05). Dietary cereal composition up-regulated jejunal TLR2 expression and interacted (P= 0·021) with dietary Ca on colonic IL1B expression; high Ca concentration up-regulated IL1B expression with wheat–barley diets and down-regulated it with maize diets. Spearman's correlations (r>0·35; P< 0·05) indicated an association between operational taxonomic units assigned to the phyla Bacteroidetes, Firmicutes and Proteobacteria and bacterial metabolites and mucosal gene expression in the colon. The present results indicate that high Ca diets have the potential to modify the jejunal and colonic mucosal gene expression response which, in turn, interacts with the composition of the basal diet and mucosa-associated bacteria in weaned pigs.

Neurocysticercosis is a public health problem in many developing countries and is the most frequent parasitic disease of the brain. The human tapeworm carrier is the main risk factor for acquiring neurocysticercosis. Since the parasite lodges only in the human intestine, experimental models of Taenia solium taeniosis have been explored. Macaques, pigs, dogs, cats and rabbits are unsuccessful hosts even in immunodepressed status. By contrast, rodents are adequate hosts since tapeworms with mature, pregravid and, in some cases, gravid proglottids develop after infection. In this review, information that has been generated with experimental models of taeniosis due to T. solium is discussed. Initially, the use of the model for immunodiagnosis of human taeniosis and evaluation of intervention measures is summarized. Next, descriptions of tapeworms and comparison of hamsters, gerbils and other mammals as experimental models are discussed, as well as data on the humoral immune response, the inflammatory reaction and the production of cytokines associated to Th1 and Th2 responses in the intestinal mucosa. Finally, evaluation of protection induced against the development of tapeworms by recombinant T. solium calreticulin in hamsters is summarized and compared to other studies.

Mouse (C3H) mucosal glycoconjugates were examined in normal small intestines and intestines infected with Echinostoma caproni, or E. trivolvis using six different fluorescein-conjugated lectins: Triticum, vulgaris agglutinin (WGA), Ulex europaeus agglutinin I (UEA-I), Ricinus communis agglutinin I (RCA-I). Glycine max soybean agglutinin (SBA), Dolichos biflorus agglutinin (DBA), and Arachis hypogaeu peanut agglutinin (PNA). The expression of lectin-binding sites and the intensity of the binding of lectins in the mouse small intestines were changed by infection with the echinostomes. Specific differences in the reaction to glycoproteins were clearly observed between the mouse intestines infected with E. caproni and those infected with E. trivolvis. In E. caproni infection, binding of most of the lectins to the villi was remarkably reduced in accord with the villous atrophy and loss of goblet cells. In contrast, in E. trivolvis infection, the binding of WGA, RCA-I and DBA was reduced in the microvillar surfaces, but binding of UEA-I and SBA were unchanged compared to the control intestines. The lectin binding to goblet cells in E. trivolvis-infected mice mostly increased. These observations may reflect the marked increase in goblet cells and the less severe damage in the villi of E. trivolvis infection compared to E. caproni infection. Most of the glycoconjugates were slightly reduced in the hyperplastic crypts except for N-acetyl glucosamine. It is possible that glucose metabolism in the host intestines infected with E. trivolvis was activated. resulting in an increase in the rate of mucin synthesis as well as qualitative changes in mucus, thereby mediating the expulsion of the worms.

In in vivo study on 24 weaned piglets (8 per group), the survival rates of human isolates Lactobacillus gasseri K7 and LF221 were quantified by selective enumeration on MRS agar with rifampicin, and the presence of both strains in intestinal mucosa was examined. Faeces from individual animals were analysed for the number (cfu/g) of coliforms, lactobacilli, clostridia and both of the two probiotic strains during 2-weeks probiotic application period (5×1010 cfu of individual strain/day) and 1 week after the probiotic treatment was ceased. Samples of duodenum, jejunum and ileum of sacrificed animals (5th or 20th day) were also examined microbiologically. A great variability in the microflora of faeces and mucosa was observed even between equally treated animals. The survival of both Lb. gasseri strains was established by their detection in the faeces (2·5×105 to 3·3×105 cfu of K7 strain/g faeces; 4·5×105 to 5×105 cfu of LF221 strain/g). In two animals, the LF221 or K7 viable cells were found in the faeces 6 d after ceasing probiotic application. In both animals from the group fed with Lb. gasseri K7 that were sacrificed 5 d after weaning, the presence of K7 strain was found either in the mucosa of duodenum (140 cfu/10 cm2) and jejunum (170 cfu/10 cm2) or in the ileum (1600 cfu/10 cm2). LF221 cells were detected in the ileal mucosa of one piglet (820 cfu/10 cm2). The results demonstrated the capability of both tested strains of in vivo adhesion to intestinal mucosa and of temporary colonisation of the piglets' intestine.

Nutritional status has a major impact on the immune system. Probiotic effects ascribed to fermented dairy products arise not only from whole microorganisms but also from metabolites (peptides, exopolysaccharides) produced during the fermentation. We recently demonstrated the immunomodulating capacity of kefir in a murine model. We now aimed at studying the immunomodulating capacity in vivo of the products derived from milk fermentation by kefir microflora (PMFKM) on the gut. BALB/c mice received the PMFKM for 2, 5 or 7 consecutive days. IgA+ and IgG+ cells were determined on histological slices of the small and large intestine. IL-4, IL-6, IL-10, IL-12, IFNγ and TNFα were determined in the gut, intestinal fluid and blood serum. IL-6 was also determined in the supernatant of a primary culture of small intestine epithelial cells challenged with PMFKM. PMFKM up-regulated IL-6 secretion, necessary for B-cell terminal differentiation to IgA secreting cells in the gut lamina propria. There was an increase in the number of IgA+ cells in the small and large intestine. The increase in the number of IgA+ cells was accompanied by an increase in the number of IL-4+, IL-10+ and IL-6+ cells in the small intestine. Effects of PMFKM in the large intestine were less widely apparent than the ones observed at the small intestine lamina propria. All cytokines that increased in the small intestine lamina propria, also did so in blood serum, reflecting here the immunostimulation achieved in the gut mucosa. We observed that the PMFKM induced a mucosal response and it was able to up and down regulate it for protective immunity, maintaining the intestinal homeostasis, enhancing the IgA production at both the small and large intestine level. The opportunity exists then to manipulate the constituents of the lumen of the intestine through dietary means, thereby enhancing the health status of the host.

Background and objective The effects of sepsis on gut mucosal blood flow have not been fully clarified. We designed an experiment to explicitly describe the effects of sepsis on gut mucosal blood flow in rats using an advanced intravital microscopy technique.

Methods This work was performed as a prospective, controlled laboratory experiment. Twenty-four hours after sham laparotomy or laparotomy and caecal ligation and perforation to create sepsis, rats were anaesthetized and their lungs mechanically ventilated (n = 7 per group). Intravital videomicroscopy was performed on 6–12 villi of ileum mucosa. Video recordings were analysed off-line using computerized image analysis.

Results Intercapillary area size (inversely related to capillary density) was increased in sepsis as compared with the control group (941 ± 92 vs. 669 ± 79 μm2, P < 0.05). In the central villus arteriole, blood flow was similar between groups (control: 3.5 ± 0.4 nL min−1; caecal ligation and perforation group: 3.6 ± 0.5 nL min−1). There were no relevant changes in arteriolar red cell velocity and diameter.

Conclusions In the gut mucosa of rats, sepsis resulting from caecal ligation and perforation depressed the perfused capillary density without affecting blood flow in the central villus arteriole. Mucosal hypoperfusion at the level of the capillary networks may occur in the presence of precapillary shunting in the villus microcirculation.

The review presents information on non-starch polysaccharides (NSPs), the major antinutritive factors found in cereals and a variety of other feed ingredients. The unique characteristics of these compounds and their effects on the utilisation of other dietary components are highlighted. The effects of NSP on the gross weight of the gastrointestinal tract, mucosal structure and function are examined and some reference is made to other species on which more research has been conducted. More research is required into the effects of NSPs on the integrity of the intestinal mucosa in poultry. Such information may assist in the development of breeding and management strategies to reduce the effects of NSPs.

In ad lib.-fed rats the epithelium of the small intestine, like the liver, contains large quantities of glutathione, 17.0 and 32.4 nmol/mg protein respectively. Following 24 h food restriction the glutathione content in both tissues fell 53 and 69% respectively. Unlike the liver, however, the glutathione content of the intestinal mucosa is not regulated to a diurnal rhythm, suggesting that the liver may provide glutathione or glutathione precursors to maintain intestinal glutathione levels. Intestinal epithelial cell preparations obtained from 24 h food-deprived rats had depleted glutathione stores (50%) and as a consequence were more susceptible to the oxidizing effects of cumene hydroperoxide. These results suggest that if glutathione plays a major role in the defence of the intestinal mucosa from ingested toxins then depletion of this defence during periods of food restriction could significantly increase the susceptibility of the individual to toxins present in the diet.