The intestinal tract is the entry gate for nutrients and symbiotic organisms, being in constant contact with external environment. DNA methylation is one of the keys to how environmental conditions, diet and nutritional status included, shape functionality in the gut and systemically. This review aims to summarise findings on the importance of methylation to gut development, differentiation and function. Evidence to date on how external factors such as diet, dietary supplements, nutritional status and microbiota modifications modulate intestinal function through DNA methylation is also presented.

The intestine plays key roles in maintaining body arginine (Arg) homoeostasis. Meanwhile, the intestine is very susceptible to reactive oxygen species. In light of this, the study aimed to explore the effects of Arg supplementation on intestinal morphology, Arg transporters and metabolism, and the potential protective mechanism of Arg supplementation in piglets under oxidative stress. A total of thirty-six weaned piglets were randomly allocated to six groups with six replicates and fed a base diet (0·95 % Arg,) or base diet supplemented with 0·8 % and 1·6 % l-Arg for 1 week, respectively. Subsequently, a challenge test was conducted by intraperitoneal injection of diquat, an initiator of radical production, or sterile saline. The whole trial lasted 11 d. The diquat challenge significantly decreased plasma Arg concentration at 6 h after injection (P<0·05), lowered villus height in the jejunum and ileum (P<0·05) as well as villus width and crypt depth in the duodenum, jejunum and ileum (P<0·05). Oxidative stress significantly increased cationic amino acid transporter (CAT)-1, CAT-2 and CAT-3, mRNA levels (P<0·05), decreased arginase II (ARGII) and inducible nitric oxide synthase mRNA levels, and increased TNF-α mRNA level in the jejunum (P<0·05). Supplementation with Arg significantly decreased crypt depth (P<0·05), suppressed CAT-1 mRNA expression induced by diquat (P<0·05), increased ARGII and endothelial nitric oxide synthase mRNA levels (P<0·05), and effectively relieved the TNF-α mRNA expression induced by diquat in the jejunum (P<0·05). It is concluded that oxidative stress decreased Arg bioavailability and increased expression of inflammatory cytokines in the jejunum, and that Arg supplementation has beneficial effects in the jejunum through regulation of the metabolism of Arg and suppression of inflammatory cytokine expression in piglets.

The gastrointestinal tract is a large reservoir of both Gram positive and negative bacteria, of which the Gram negative bacteria act as a source of lipopolysaccharide (LPS). Luminal LPS, commonly known as endotoxin, can enter systemic circulation via paracellular and transcellular permeation. It has been shown that endotoxin exposure can increase intestinal paracellular permeability and alter intestinal structure and function, resulting in impaired absorption and utilisation of nutrients with negative impact on both poultry heath and growth. Acute exposure to large amounts of endotoxin suppresses feed intake in chickens and activation of the innate immune system. Substantial evidence suggests that endotoxin is recognised via toll-like receptor (TLR)-4, located on the surface of immune cells, which activates kinases to enhance the transcription of pro-inflammatory cytokines such as tumour necrosis factor alpha (TNF-α) and interleukin (IL)-1 and 6 which mediate the inhibitory effect of endotoxin on the intestinal nutrient absorption. Inflammation can divert energy and nutrients away from growth supp and into supporting the immune system responses, leading to growth suppression and lowered feed efficiency. In addition, sustained exposure to endotoxin may elicit tolerance, which can make animals refractory against secondary Gram-negative infections. In this review, the effects of endotoxin on intestinal barrier functions and the subsequent negative impacts on the production of chickens are summarised. Overall, this review combines the current knowledge of the chicken's intestinal responses to Gram negative bacterial infection, illustrating the importance of gut health in defence against bacterial infections and improving poultry health, growth and welfare.

Intra-uterine growth-retarded (IUGR) neonates have shown an impairment of postnatal intestinal development and function. We hypothesised that the immune function of IUGR neonates might be affected by increased nutrient intake (NI) during the suckling period. Therefore, we investigated the effects of high NI (HNI) on the growth performance, intestinal morphology and immunological response of IUGR and normal-birth weight (NBW) piglets. A total of twelve pairs of IUGR and NBW piglets (7 d old) were randomly assigned to two different nutrient-level formula milk groups. After 21 d of rearing, growth performance, the composition of peripheral leucocytes, serum cytokines and intestinal innate immune-related genes involved in the Toll-like receptor (TLR)-4–myeloid differentiation factor 88–NF-κB pathway were determined. The results indicated that IUGR decreased the average daily DM intake (ADMI) and the average daily growth (ADG). However, the ADMI and ADG were increased by HNI, irrespective of body weight. Likewise, serum cytokines (TNF-α and IL-1β) and ileal gene expressions (TLR-4, TLR-9, TRAF-6 and IL-1β) were lower in IUGR piglets, whereas HNI significantly increased blood lymphocyte percentage and serum IL-10 concentrations, but decreased neutrophil percentage, serum IL-1β concentrations and ileal gene expressions (NF-κB and IL-1β). Furthermore, IUGR piglets with HNI exhibited lower serum concentrations of TNF-α and IL-1β than NBW piglets, and these alterations in the immune traits of IUGR piglets receiving HNI were accompanied by decreasing ileal gene expressions of TLR-4, TLR-9, NF-κB and IL-1β that are related to innate immunity. In conclusion, the present findings suggest that increased NI during the suckling period impaired the immune function of neonatal piglets with IUGR.

High dietary threonine extraction by the digestive tract suggests that threonine contributes to maintain gut integrity. The aims of this study were to investigate the intestine development and the growth performance of early-weaned piglets pair-fed either a control well-balanced (C: 9.3 g threonine/kg diet) or a low-threonine diet (LT: 6.5 g threonine/kg diet) for 2 weeks. As expected, LT piglets presented lower plasma free threonine compared with C piglets (118 v. 356 ± 12 μmol/l, P < 0.001). Dietary threonine supply altered neither growth performance nor growth of the intestine and of the other portal-drained viscera (stomach, spleen and pancreas). Nevertheless, villus height was reduced in the ileum of the LT piglets compared with C piglets (446 v. 714 ± 74 μm, P < 0.05). This was also associated with a decrease in crypt width (P < 0.05) and villus height-to-crypt depth ratio (P < 0.05). Whereas maltase and lactase activities did not change between the two groups, aminopeptidase nitrogen activity was decreased in the ileum of LT piglets (269 v. 374 ± 27 IU/mg protein, P < 0.05). The number of mucin-containing goblet cells was not modified in the ileum and in the proximal part of the large intestine of the LT piglets compared with the C piglets. In conclusion, despite no alteration of intestinal growth, villus hypotrophy associated with a reduction of aminopeptidase nitrogen activity suggest an alteration of the structure of the ileum in early-weaned piglets fed a diet supplying inadequate dietary threonine.

The objective of this study was to investigate the effect of orally administered spermine at various doses on intestinal maturation in sucking piglets. Thirty-six 11-day-old sucking piglets were assigned randomly to one of six treatments to receive via a stomach tube 0, 0·1, 0·2, 0·3, 0·4, or 0·5 mmol spermine per kg live weight (LW) per day for 3 days. At day 14 of age, duodenum, jejunum and ileum were obtained for biochemical and morphological analysis. Increasing the dose of orally administered spermine increased intestinal weight (linear effect, P<0·01), mucosal weight (linear effect, P<0·05), and mucosal protein, DNA and RNA contents of the duodenum (linear effect, P≤0·01) and jejunum (linear effect, P<0·01). Elevating spermine doses also enhanced (linear effect, P≤0·02) the specific activities of maltase and sucrase but decreased (linear effect, P<0·01) lactase specific activity in the jejunum and duodenum. Furthermore, augmenting oral doses of spermine increased crypt depth and villus width but reduced villus height in the jejunum (linear effect, P<0·05) and duodenum (linear effect, P<0·01). For most measurements, the effects were observed at the oral spermine doses of 0·3 to 0·5 mmol/kg LW per day. Collectively, the results show that oral administration of optimal doses of spermine to 11-day-old sucking piglets induces precocious intestinal maturation and promotes intestinal growth.

Sixteen pigs (eight entire males and eight females) were given individually two diets, control and control added 25% chopped chicory roots for 2 months before slaughter. Samples were taken from the contents in colon and rectum and subjected to GC-MS analysis for amount of odour impact compounds. The compounds 2-pentanone, ethylbutyrate, propylpropionate, butyric acid, ethyl-2-methylbutyrate, p-cresol, indole and skatole showed a significant difference between the two treatments. The esters, which have relatively pleasant, often fruity odours, increased in the chicory treatment, whereas the malodorous compounds, p-cresol, indole and skatole decreased in the chicory treatment. The measured amounts of compounds were corrected for their odour thresholds as different compounds can have widely different odour thresholds. Principal components analysis was then used to analyse the raw and corrected data results. p-Cresol was the most malodorous compound and together with skatole and indole count as the most malodorous compounds in the colon and rectum cotents. However, butyric acid also had some minor influence. Feeding chicory roots decreased significantly the concentrations of these malodorous compounds, especially if the lowest odour threshold values are used as correction factors.

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.