Interleukin-10 is differentially expressed in the small intestine and the colon experiencing chronic inflammation and ulcerative colitis induced by dextran sodium sulfate in young pigs.

Intestinal inflammation induced with dextran sodium sulfate (DSS) is used to study acute or chronic ulcerative colitis in animal models. Decreased gut tissue anti-inflammatory cytokine IL-10 concentration and mRNA abundance are associated with the development of chronic bowel inflammation. Twelve piglets of 3 days old were fitted with an intragastric catheter and randomly allocated into control and DSS groups by administrating either sterile saline or 1.25 g of DSS/kg body weight (BW) in saline per day, respectively, for 10 days. Growth rate and food conversion efficiency were reduced (p<0.05) in the DSS piglets compared with the control group. Quantitative histopathological grading of inflammation in the jejunum and colon collectively showed that the DSS treatment resulted in 12 fold greater (p<0.05) inflammation severity scoring in the colon than in the jejunum, indicative of chronic ulcerative colitis in the colon. Upper gut permeability endpoint was 27.4 fold higher (p<0.05) in the DSS group compared with the control group. The DSS group had higher concentrations and mRNA abundances (p<0.05) of TNF-alpha and IL-6 in the jejunal and colonic tissues compared with the control group. Colonic concentration and mRNA abundance of IL-10 were reduced (p<0.05), however, jejunal IL-10 mRNA abundance was increased (p<0.05) in the DSS group compared with the control group. In conclusion, administration of DSS at 1.25 g/kg BW for 10 days respectively induced acute inflammation in the jejunum and chronic inflammation and ulcerative colitis in the colon with substantially decreased colonic concentration and mRNA abundance of IL-10 in the young pigs, mimicking the IL-10 expression pattern in humans Associated with chronic bowel inflammation.

Consumption of guar gum and retrograded high-amylose corn resistant starch increases IL-10 abundance without affecting pro-inflammatory cytokines in the colon of pigs fed a high-fat diet.

Increases in dietary intake of viscous and nonviscous soluble fiber are reported to improve bowel health. However, related biological mechanisms are not very clear. This study was conducted to examine if colonic inflammation would occur in a typical Western diet model and determine if consumption of soluble fiber components would attenuate potential detrimental effects by differentially affecting colonic abundances of anti-inflammatory cytokine IL-10 and 2 pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α) and IL-6 in pigs fed a high-fat basal diet supplemented, respectively, with 15% viscous soluble fiber guar gum (GG) and 15% nonviscous soluble fiber, that is, retrograded high-amylose corn (Zea mays) resistant starch (RS). A total of 24 Yorkshire growing barrows were assigned into a standard corn and soybean (Glycine max) meal (SBM)-based grower diet as a positive control (PC), an animal protein-based high-fat basal diet as the negative control (NC), and 2 NC basal diets supplemented with 15% GG and 15% RS, respectively, according to a completely randomized block design for 4 wk. Abundance of these cytokines in homogenized and extracted colonic tissue supernatant samples was measured by ELISA. Although colonic IL-10 abundance was lower (P < 0.05) in the corn and SBM-based PC group than that in the high-fat basal NC group, there were no differences (P > 0.05) in colonic abundances of TNF-α and IL-6 between NC and PC groups and among all of the treatment groups. Compared with the NC group, consumption of GG and RS at 15% increased (P < 0.05) colonic IL-10 abundance. Moreover, there was no difference (P > 0.05) in colonic IL-10 abundance between the 15% GG and the 15% RS groups. Thus, consumption of a typical high-fat Western diet did not induce colonic inflammation. Diets supplemented with 15% GG or 15% RS may protect the colon from developing inflammation by enhancing IL-10 abundance.

The small intestinal apical hydrolase activities are decreased in the piglet with bowel inflammation induced by dextran sodium sulfate.

Inflammatory bowel disease (IBD) is characterized by cramping, abdominal pain, bloating, constipation, and diarrhea. We tested the hypothesis that compromised activities of the major small intestinal apical hydrolases contribute to the symptoms of IBD. Changes in hydrolytic kinetics, target protein abundances, and mRNA expression of intestinal alkaline phosphatase (IAP), lactase, maltase, sucrase-isomaltase (SI), maltase-glucoamylase (MGA), and aminopeptidase N (APN) in piglets with colonic inflammation chemically induced by dextran sodium sulfate (DSS) were investigated. Yorkshire piglets at 5 d of age, with an average initial BW of about 3 kg, were fitted with intragastric catheters and were divided into control (CON; n = 6) and treatment groups (DSS; n = 5). Both groups were infused with an equal volume of either saline or 1.25 g of DSS · kg BW(-1) · d(-1) in saline, respectively, for 10 d. Enzyme kinetic experiments for IAP, lactase, maltase, SI, MGA, and APN were measured at 37°C with isolated proximal jejunal apical membrane. Target hydrolase protein abundances in the apical membrane were analyzed by Western blotting and their mRNA abundances in the jejunum were measured by quantitative real-time reverse transcription (RT-) PCR with ß-actin as the housekeeping gene. Expressed as percentage of the CON, DSS treatment decreased (P < 0.05) the maximal specific activities of IAP (53%), lactase (78%), maltase (56%), SI (72%), MGA (29%), and APN (22%) as well as the target hydrolase protein abundances of IAP (39%), lactase (35%), SI (36%), and APN (54%), respectively. Decreases (P < 0.05) in the mRNA abundances (% of the CON) for lactase (25%), SI (52%), MGA (75%), and APN (39%) were observed in the DSS group. However, DSS treatment increased (P < 0.05) the jejunal IAP mRNA abundance by 3.5 fold. We conclude that decreases in the small intestinal apical activities of these examined hydrolases likely contribute to overgrowth of pathogenic bacterial populations in the distal small intestine and the colon, leading to the pathogenesis of IBD.

The in vivo infusion of hydrogen peroxide induces oxidative stress and differentially affects the activities of small intestinal carbohydrate digestive enzymes in the neonatal pig.

Chronic fatigue syndrome (CFS) is characterized by persistent and relapsing fatigue that involves oxidative stress in its pathogenesis. We tested the hypothesis that a decrease in key carbohydrate-digesting enzyme activity in the gut is one of the major biological mechanisms of developing CFS in liquid formula-fed neonatal pigs with in vivo infusion of H(2)O(2). Piglets at 7 to 10 d of age were fitted with an intraperitoneal catheter, allowed a 3-d post surgical recovery, and infused with either H(2)O(2) at 5 mmol/kg BW (PER; n = 8) or the same volume of saline (CON; n = 8) in six 20-ml doses daily for a period of 10 d. During this period, animal behavior was monitored, blood samples collected, and jejunal enzyme activity kinetic experiments for lactase, sucrase, maltase, and maltase-glucoamylase were conducted. Plasma concentration of reduced glutathione remained similar (P > 0.05) to the pre-infusion level over the study duration in the CON group whereas this was 65% lower (P < 0.05) than the pre-infusion level in the PER group. Piglets experiencing oxidative stress had an overall lower (P < 0.05) physical mobility and the maximal jejunal specific activities [µmol/(mg protein · min)] for lactase (PER, 6.54 ± 0.68 vs. CON, 12.65 ± 0.69) and maltase (PER, 57.39 ± 1.02 vs. CON, 75.60 ± 1.04), respectively. However, differences were not observed (P > 0.05) in the maximal specific activities [µmol/(mg protein · min)] of sucrase (PER, 10.50 ± 1.37 vs. CON, 12.40 ± 1.55) and maltase-glucoamylase (PER, 0.71 ± 0.08 vs. CON, 0.70 ± 0.07) between the 2 groups. In conclusion, infusion of a suitable dose of H(2)O(2) induced CFS in the neonatal pigs. Oxidative stress in vivo differentially affected the maximal activities of important small intestinal carbohydrate-digesting enzymes in neonatal pigs fed a dairy milk-based liquid formula.

Novel methodology allows simultaneous measurement of true phosphorus digestibility and the gastrointestinal endogenous phosphorus outputs in studies with pigs.

Methodology was developed for measuring the gastrointestinal endogenous phosphorus (P) outputs and true P digestibility values in studies with piglets. Four barrows, average initial body weight 6.8 kg, were fitted with a simple T-cannula at the distal ileum and fed four diets according to a 4 x 4 Latin square design. Four cornstarch-based diets containing four levels of P (1.1, 2.1, 3.2 and 4.3 g/kg diet) on a dry matter (DM) basis were formulated from soybean meal (SBM). Each experimental period comprised 8 d with a 4-d adaptation and 4-d collection of ileal digesta and feces. The apparent ileal and fecal P digestibility values in SBM were affected (P < 0.05) by P levels in the assay diets. The ileal and fecal P digestibility values increased from -24.8 to 37.1% and from 18.8 to 42.5%, respectively, as P contents increased from 1.1 to 4.3 g/kg DM diet. Linear relationships (P < 0.05), expressed as g/kg DM diet intake, between ileal and fecal outputs and dietary inputs of P, suggested that the endogenous P outputs can be determined by linear regression analysis. The endogenous P output was higher (P < 0.05) in ileal digesta than in feces (0.86 +/- 0.09 vs. 0.31 +/- 0.06 g/kg DM diet intake). There was no difference (P > 0.05) between the true ileal (50.7 +/- 7.1%) and fecal (48.5 +/- 5.4%) P digestibility values in SBM. These results suggest that differences in P contents between assay diets are primarily responsible for the large variability in apparent P digestibility values reported within the same ingredient. Apparent digestibility values underestimate the true digestive utilization of P by approximately 25%. True rather than apparent P digestibility values should be determined and used in diet formulation for pigs. In addition, this study shows that the gastrointestinal endogenous P output is important in whole-body P requirement and homeostasis.