Intestinal Physiological Functions Research Articles

Sanguinarine Improves Intestinal Health in Grass Carp Fed High-Fat Diets: Involvement of Antioxidant, Physical and Immune Barrier, and Intestinal Microbiota.

An eight-week trial was conducted to investigate the effects of sanguinarine supplementation (600 μg and 1200 μg/kg) in high-fat (crude fat: 10%) diets (HF) on the intestinal physiological function of Ctenopharyngodon idellus (initial weight 50.21 ± 0.68 g), based on a basic diet (5% crude fat, CON), which were named HFLS and HFHS, respectively. The results showed that the HF diet significantly impaired the intestinal immune and physical barrier function, and disrupted the balance of the intestinal microbiota in grass carp. Compared to the HF diet, sanguinarine supplementation significantly improved the levels of serum C4, C3, AKP, IgA, and IgM, and enhanced the intestinal antioxidant capacity (gr, CuZnsod, gpx4, cat, gsto, and nrf2 expression were significantly up-regulated). Sanguinarine significantly down-regulated the expression of claudin-15 and up-regulated the expression of claudin-b, claudin-c, occludin, and zo-1 by inhibiting MLCK signaling molecules. Additionally, sanguinarine significantly down-regulated the expression of il-6, il-1β, and tnf-α and up-regulated the expression of il-10, tgf-β2, and tgf-β1 by inhibiting NF-κB signaling molecules, thereby alleviating intestinal inflammation caused by HF diets. Furthermore, compared to the HF diet, the abundance of Fusobacterium and Cetobacterium in the HFHS diet increased significantly, while the abundance of Firmicutes and Streptococcus showed the opposite trend. In conclusion, the HF diet had a negative impact on grass carp, while sanguinarine supplementation enhanced intestinal antioxidant ability, alleviated intestinal barrier damage, and ameliorated the homeostasis of the intestinal microbiota.

The protective effects of Bacillus licheniformis against inflammatory responses and intestinal barrier damage in broilers with necrotic enteritis induced by Clostridium perfringens.

Bacillus licheniformis is a gram-positive bacterium that has strong environmental adaptability and can improve the growth performance, immunity, and antioxidant function of broilers. The current study aimed to elucidate the protective capability of B. licheniformis against inflammatory responses and intestinal barrier damage in broilers with necrotic enteritis (NE) induced by Clostridium perfringens (CP). The results showed that B. licheniformis enhanced the final body weight in broilers compared with that of broilers in the CP group after the stress of infection (P < 0.05). Bacillus licheniformis reversed the decreased levels of serum and jejunum mucosa immunoglobulins and anti-inflammatory cytokines, reduced the values of villus height and the ratio of villus height to crypt depth, and mitigated the increased levels of serum d-lactic acid and diamine oxidase in CP-challenged broilers (P < 0.05). Moreover, B. licheniformis modulated the expression levels of genes involved in the TLR4/NF-κB signalling pathway, the NLRP3 inflammasome activation pathway, and the sirt 1/Parkin signalling pathway in CP-challenged broilers. Compared with the CP challenge group, the B. licheniformis-treated group exhibited reduced abundance values of Shuttleworthia and Alistipes and enhanced abundance values of Parabacteroides in the caecal contents (P < 0.05). Bacillus licheniformis improved the final body weight and alleviated the inflammatory response and intestinal barrier function damage in birds with NE induced by CP by maintaining intestinal physiological function, enhancing immunity, regulating inflammatory cytokine secretion, modulating the mitophagy response, and increasing the abundance of beneficial intestinal flora. © 2023 Society of Chemical Industry.

The Effect of Buckwheat Resistant Starch on Intestinal Physiological Function.

Resistant starch appears to have promising effects on hypertension, cardiovascular and enteric illness. The influence of resistant starch on intestinal physiological function has drawn great attention. In this study, we first analyzed the physicochemical characteristics, including the crystalline properties, amylose content, and anti-digestibility among different types of buckwheat-resistant starch. The influence of resistant starch on the physiological functions of the mouse intestinal system, contained defecation, and intestinal microbes were also evaluated. The results showed that the crystalline mold of buckwheat-resistant starch changed from A to B + V after acid hydrolysis treatment (AHT) and autoclaving enzymatic debranching treatment (AEDT). The amylose content in AEDT was higher than in AHT and raw buckwheat. Moreover, the anti-digestibility of AEDT was also stronger than that in AHT and raw buckwheat. The buckwheat-resistant starch can promote bowel intestinal tract movement. The quantity of intestinal microbe was regulated by buckwheat-resistant starch. Our research demonstrates an effective preparation method for improving the quality of buckwheat-resistant starch and found that buckwheat-resistant starch has the role of adjusting the distribution of the intestinal flora and maintaining the health of the body.

Research Progress on Lycopene in Swine and Poultry Nutrition: An Update.

Oxidative stress and in-feed antibiotics restrictions have accelerated the development of natural, green, safe feed additives for swine and poultry diets. Lycopene has the greatest antioxidant potential among the carotenoids, due to its specific chemical structure. In the past decade, increasing attention has been paid to lycopene as a functional additive for swine and poultry feed. In this review, we systematically summarized the latest research progress on lycopene in swine and poultry nutrition during the past ten years (2013-2022). We primarily focused on the effects of lycopene on productivity, meat and egg quality, antioxidant function, immune function, lipid metabolism, and intestinal physiological functions. The output of this review highlights the crucial foundation of lycopene as a functional feed supplement for animal nutrition.

PSX-A-5 Effects of High- and low-Fiber Diets on Growth Performance and Intestinal Oxidative Stress in Growing-Finishing Pigs

Abstract Feed is the most expensive input in commercial pork production. In order to reduce feed costs, using high-fiber ingredients has become a common practice. Moderate levels of fiber can maintain intestinal physiological function and promote intestinal health. Oxidative stress is linked to impaired nutrient absorption and growth performance. This study investigated the effects of high-fiber (HF, 6% crude fiber) and low-fiber (LF, 3% crude fiber) diets on growth performance and intestinal oxidative stress parameters in growing-finishing pigs. Forty growing pigs (27.07 ± 1.26 kg BW) were randomly assigned to 2 treatments with 10 replicates of 2 pigs per pen. Pigs were weighed on days 35, 42 and 70. The feed intake was recorded daily to calculate growth performance parameters. On day 70, eight pigs in each treatment group were randomly selected and euthanized to obtain jejunum to measure oxidative stress status. Pigs fed an HF diet were heavier than those fed an LF diet on days 35, 42 and 70 (P &amp;lt; 0.05). During the whole feeding period, pigs fed an HF diet had higher average daily gain than those fed an LF diet (P &amp;lt; 0.05). The LF diet resulted in increased levels of malondialdehyde (P &amp;lt; 0.05) in the jejunum, suggesting that the LF diet contributed to oxidative stress in the jejunum. The LF diet also led to a significant increase in glutathione and oxidized glutathione levels (P &amp;lt; 0.05) in the jejunum, indicating that pigs fed an LF diet needed to produce more antioxidant substances to cope with oxidative stress in the intestine. This was accompanied by a significant increase in glutamate-cysteine ligase in the jejunum of the LF group (P &amp;lt; 0.05). These results suggest that the HF diet can improve growth performance and maintain intestinal health in growing-finishing pigs by reducing intestinal oxidative stress.

Effects of high- and low-fiber diets on intestinal oxidative stress in growing-finishing pigs.

Feed is the most expensive facet of commercial pork production. In order to reduce feed costs, using high-fiber ingredients has become a common practice. Moderate levels of fiber can maintain intestinal physiological function and promote intestinal health. Oxidative stress is linked to impaired nutrient absorption and growth performance. This study investigated the effects of high-fiber (5.26% crude fiber) and low-fiber (2.46% crude fiber) diets on growth performance and intestinal oxidative stress parameters in growing-finishing pigs. Forty growing pigs with initial body weight (27.07 ± 1.26 kg) were randomly assigned to 2 treatment groups with 10 replicates of 2 pigs per pen. Pigs were weighed on day 35, 42, and 70. The feed intake was recorded daily to calculate growth performance parameters. On day 70, eight pigs in each treatment group were randomly selected and euthanized to obtain jejunum to measure oxidative stress status. Pigs fed a high-fiber diet were heavier than those fed a low-fiber diet on days 35, 42, and 70 (P < 0.05). During the whole feeding period, pigs fed a high-fiber diet had a higher average daily gain than those fed a low-fiber diet (P < 0.05). The low-fiber diet resulted in increased levels of malondialdehyde (P < 0.05) in the jejunum, suggesting that the low-fiber diet contributed to oxidative stress in the jejunum. The low-fiber diet also led to a significant increase in glutathione and oxidized glutathione levels (P < 0.05) in the jejunum, indicating that pigs fed a low-fiber diet needed to produce more antioxidant substances to cope with oxidative stress in the intestine. This was accompanied by a significant increase in the expression of glutathione synthesizing enzymes in the jejunum of the low-fiber group (P < 0.05). These results suggest that the high-fiber diet can improve growth performance and maintain intestinal health in growing-finishing pigs by reducing intestinal oxidative stress.

Heat Stress Decreases Intestinal Physiological Function and Facilitates the Proliferation of Harmful Intestinal Microbiota in Sturgeons

Heat is a common source of stress in aquatic environments and can alter the physiological and metabolic functions of aquatic animals, especially their intestinal function. Here, the effects of heat stress on the structure and function of the intestine and the characteristics of the intestinal microbiota were studied in sturgeon (Acipenser baerii ♀ × Acipenser schrenckii ♂ hybrid F1). Sturgeons were exposed to sub-extreme (24°C) and extreme (28°C) high water temperatures for 12 days. The heat stress caused systemic damage to the intestine of sturgeons, which displayed severe enteritis in the valve intestine. The microbial diversity analysis showed that heat stress led to the disorder in intestinal microbiota, manifesting as an explosive increase in the abundance of thermophilic intestinal pathogens such as Plesiomonas, Cetobacterium, and Aeromonas and causing physiological dysfunction in the sturgeons. The disorder was followed by significant inhibition of intestinal digestion with reduced chymotrypsin, α-amylase, and lipase activities in the valve intestine and of antioxidant function with reduced peroxidase (POD) and catalase (CAT) activities. Simultaneously, heat stress reduced the thermal tolerance of sturgeons by reducing Grp75 expression and damaged the valve intestine’s repair ability with increased Tgf-β expression. The results confirmed that heat stress damaged the sturgeon intestines obviously and disturbed the intestinal microbiota, resulting in serious physiological dysfunction. The present study investigated the mechanism of the effect of heat stress on the sturgeon intestine and will help develop strategies to improve the resistance to thermal stress for wild and cultured sturgeons.

Resveratrol alleviates enterotoxigenic Escherichia coli K88-induced damage by regulating SIRT-1 signaling in intestinal porcine epithelial cells.

This study found that resveratrol pretreatment attenuated porcine intestinal epithelial cell damage caused by enterotoxigenic Escherichia coli (ETEC) K88 in vitro and the protective effects of resveratrol were associated with SIRT-1 signaling. ETEC K88 is a main intestinal pathogen for post-weaning diarrhea (PWD) in piglets. With the strict ban on antibiotics in animal feed, people are seeking effective antibiotic substitutes to protect the intestinal system against harmful pathogenic bacteria. This study was conducted to evaluate the effects of resveratrol, a natural plant polyphenol, on ETEC K88-induced cellular damage in porcine enterocytes and underlying mechanisms. Intestinal porcine epithelial cell line 1 (IPEC-1) cells, pretreated with or without resveratrol (30 μM, 4 h), were challenged with ETEC K88 (MOI = 1 : 10) for 3 h. The results showed that ETEC K88 infection induced severe damage and dysfunction in IPEC-1 cells, as evidenced by a reduced cell viability, decreased tight junctions, mitochondrial dysfunction, and autophagy. It is noteworthy that IPEC-1 cells pre-treated with resveratrol improved their capacity for resistance to most of these abnormal phenotypes caused by ETEC K88 infection. Furthermore, we found that the activation of SIRT-1 signaling was associated with the benefits of resveratrol, as demonstrated by EX-527, an inhibitor of SIRT-1, which reversed most of the protective effects of resveratrol. In conclusion, these results indicated that resveratrol could protect intestinal epithelial cells against ETEC K88 infection by activating SIRT-1 signaling. These findings provide new insights into the role of resveratrol in maintaining intestinal physiological functions.

The Roles of Prebiotics on Impaired Immune System in Preterm Infants: A Narrative Literature Review

ABSTRACT Background: After birth, preterm infants face numerous challenges, including short and long-term morbidities, to survive and grow well with impaired immune and gastrointestinal systems. According to data from 184 countries, preterm birth rate ranges from 5-18%, accounting for 35% of all new born deaths. Purpose: This literature review aimed to summarize the evidence for the impact of prematurity on immune system development and the benefit of prebiotics on gut microbiota and immune responses. Discussion: Various studies in this narrative literature review showed that preterm infants have both qualitative and quantitative immune response deficits compared to term infants. Preterm newborns also have impaired intestinal immunity, underdeveloped intestinal mucosa barrier, and gut dysbiosis, which predisposes them to life-threatening infections. Early balanced gut microbiota in infants believed to be essential for adequate intestinal physiological functions and immune system maturation. The use of prebiotics, including human milk oligosaccharides (HMOs) in human breast milk, has been found to decrease the risk of various infections and cognitive impairment. A previous study found that prebiotic oligosaccharides supplementation was well-tolerated, significantly increased Bifidobacteria growth, and reduced the presence of gut pathogens. Conclusions: There was robust evidence that breast milk and prebiotics supplementation may support the gut microbiome and immune system in preterm infants. However, different types of synthetic prebiotics offer different benefits, and the protective effect seems to depend on the supplementation duration and dosage.

Toxic effects of ammonia on the intestine of the Asian clam (Corbicula fluminea)

Intestines contain a large number of microorganisms that collectively play a vital role in regulating physiological and biochemical processes, including digestion, water balance, and immune function. In this study, we explored the effects of ammonia stress on intestinal inflammation, the antioxidant system, and the microbiome of the Asian clam (Corbicula fluminea). Exposure to varying ammonia concentrations (10 and 25 mg N/L) and exposure times (7 and 14 days) resulted in damage to C. fluminea intestinal tissue, according to histological analysis. Furthermore, intestinal inflammatory responses and damage to the antioxidant system were revealed through qPCR, ELISA, and biochemical analysis experiments. Inflammatory responses were more severe in the treatment group exposed to a lower concentration of ammonia. High-throughput 16S rDNA sequencing showed that ammonia stress under different conditions altered intestinal bacterial diversity and microbial community composition, particularly impacting the dominant phylum Proteobacteria and genus Aeromonas. These results indicate that ammonia stress can activate intestinal inflammatory reactions, damage the intestinal antioxidant system, and alter intestinal microbial composition, thereby impeding intestinal physiological function and seriously threatening the health of C. fluminea.

Procyanidin B2 Promotes Intestinal Injury Repair and Attenuates Colitis-Associated Tumorigenesis via Suppression of Oxidative Stress in Mice.

Aims: Intact intestinal epithelium is essential to maintain normal intestinal physiological function. Irradiation-induced gastrointestinal syndrome or inflammatory bowel disease occurred when epithelial integrity was impaired. This study aims at exploring the mechanism of procyanidin B2 (PB2) administration to promote intestinal injury repair in mice. Results: PB2 treatment reduces reactive oxygen species (ROS) accumulation and protects the intestine damage from irradiation. Mechanistic studies reveal that PB2 could effectively slow down the degradation of nuclear factor-erythroid 2-related factor 2 (Nrf2) and it significantly triggers Nrf2 into the nucleus, which leads to subsequent antioxidant enzyme expression. However, knockdown of Nrf2 attenuates PB2-induced protection in the intestine. More importantly, PB2 also promotes leucine-rich repeat-containing G protein-coupled receptor 5 (Lgr5)-positive intestinal stem cells (Lgr5+ ISCs) driven regeneration via enhancing Wnt/β-catenin signaling, which depends on, at least in part, activation of the Nrf2 signal. Evidence from an injury model of intestinal organoids is similar with in vivo results. Correspondingly, results from flow cytometric analysis and luciferase reporter assay reveal that PB2 also inhibits the level of ROS and promotes Lgr5 expression in vitro. Finally, PB2 alleviates the severity of experimental colitis and colitis-associated cancer in a long-term inflammatory model via inhibiting nuclear localization of p65. Innovation: This study, for the first time, reveals a role of PB2 for intestinal regeneration and repair after radiation or dextran sulfate sodium-induced injury in mice. Conclusion: Our results indicate that PB2 can repress oxidative stress via Nrf2/ARE signaling and then promote intestinal injury repair.

PSVIII-6 The small intestinal responses in the determination of true digestibility and the endogenous outputs of phosphorus in corn for growing pig using the regression analysis technique

Abstract It is of important methodological considerations to understand how the small intestine would respond to feeding of a series of assay diets deficient in gradient levels of phosphorus (Pi) associated with corn in growing pigs by the regression analysis technique (TRAT). A total of 48 barrows, with an average initial BW 32 kg, were randomly assigned to 6 grower pig diets and were fed close to ad libitum for 10 d, with 8-d adaptation and 2-d collection fecal samples, according to a randomized complete block design. Six cornstarch-based diets, containing 6 levels of Pi at 1.3, 1.9, 2.0, 3.6, 3.4 and 4.0 g/kg DMI, were formulated from corn. The gut permeability marker of D-mannitol was fed 0.30 g/kg BW at 4 h, prior to be sacrificed for sampling. ADG and the apparent ileal DM digestibility were linearly affected (P &amp;lt; 0.05); however, the ADFI, feed conversion ratio, the apparent fecal DM digestibility, transcellular gut permeability and the jejunal alkaline phosphatase kinetics were not affected (P &amp;gt; 0.05) by the increasing dietary levels of corn inclusion. There were linear relationships (P &amp;lt; 0.05), expressed as g/kg DMI, between the apparent ileal and fecal digestible Pi and the total intake of dietary Pi, suggesting that true ileal and fecal Pi digestibility (33.3±4.7 vs. 52.7±3.8%); and the endogenous Pi outputs (0.37±0.12 vs. 0.60±0.09, g/kg DMI) associated with corn could be estimated by the TRAT. Our results have shown that the intestinal physiological functions were not affected in the grower pigs fed on a series of test diets that were deficient in gradient levels of multiple assay nutrients, including macro-minerals, crude protein and amino acids supplied from the testing corn, for a period of 10 d, in the determination of corn-specific true digestibility and the endogenous outputs of Pi by the TRAT.

PSI-5 Intestinal responses and the determination of true total tract trace mineral digestibility and the endogenous losses in weanling pigs by the regression analysis technique

Abstract There is limited knowledge regarding trace mineral bioavailability in trace mineral supplements and common feed ingredients and trace mineral endogenous losses in pigs. The objectives of this study were to investigate intestinal responses and to determine true total tract trace mineral digestibility and the endogenous losses of trace minerals associated with corn and SBM based diets in weanling pigs by the regression analysis. Twenty-four crossbred barrows, with an average initial BW of 14 kg, were randomly assigned to 4 weanling pig diets with inclusion of titanium dioxide (0.30%) and a commercial trace mineral-vitamin premix at 0.125, 0.250, 0.375 and 0.500%, respectively, to result in 4 graded dietary levels of Cu, Zn, Fe, Mn and Se. The pigs were fed close to ad libitum for 11 d according to a randomized complete block design. The dietary inclusion did not affect (P &amp;gt; 0.05) growth performances, ileal and fecal DM digestibility, D-mannitol gut permeability and jejunal alkaline phosphatase kinetics. With the regression analysis, true total tract Cu, Zn, Fe, Mn and Se digestibility values (±SE; n = 23 or 24; P &amp;lt; 0.05) in the trace mineral-vitamin premix were determined to be 137.3±27.9, 40.5±15.4, 66.2±24.6, 94.3±21.6 and 96.6±2.8% vs. the corresponding values in the four weanling pig diets for Cu at 137.4±3.2, Zn at 40.4±3.1, Fe at 66.2±3.0, Mn at 94.2±3.8and Se at 96.2±0.8%, respectively. The total tract endogenous Cu, Zn, Fe, Mn and Se outputs (±SE)associated with the weanling pig diets were also determined (23.4±0.6, 9.2±2.7, 37.2±3.5, 19.4±1.0 and 0.07±0.003 mg/kg DMI diets; n = 23 or 24;P &amp;lt; 0.05). Our results have shown that the intestinal physiological functions and performances were not significantly affected in the weanling pigs fed on the diets with reduced gradient levels of a trace mineral-vitamin premix. Total tract true digestible trace mineral supply should be considered in swine diet formulation.

Benzoic Acid Used as Food and Feed Additives Can Regulate Gut Functions.

As a kind of antibacterial and antifungal preservative, benzoic acid is widely used in foods and feeds. Recently, many studies showed that it could improve the growth and health, which should, at least partially, be derived from the promotion of gut functions, including digestion, absorption, and barrier. Based on the similarity of gut physiology between human and pigs, many relative studies in which piglets and porcine intestinal epithelial cells were used as the models have been done. And the results showed that using appropriate benzoic acid levels might improve gut functions via regulating enzyme activity, redox status, immunity, and microbiota, but excess administration would lead to the damage of gut health through redox status. However, the further mechanisms that some intestinal physiological functions might be regulated are not well understood. The present review will, in detail, summarize the effect of benzoic acid on gut functions.

Prophylactic use of probiotic chocolate modulates intestinal physiological functions in constipated rats.

This study investigated the in vivo prophylactic effect of probiotic chocolate on constipation. Rats were administered chocolate containing 2.5×1010 CFU g-1 of probiotics daily for 4 weeks and treated with loperamide (5 mg kg-1 ) daily at the fourth week of treatment. Probiotic chocolate treatment significantly (P<0.05) increased the intestinal motility, colon length, fecal moisture content and number of excreted fecal pellets in constipated rats. Moreover, quantitative real-time polymerase chain reaction data and histological images also revealed that both probiotic chocolate LYC and BB12 treatments were capable of upregulating the mRNA expression levels of colonic ZO-1, occludin and AQP8, leading to the maintenance of the defensive barrier function in the constipated rats compared with the negative controls. Interestingly, these treatments also modulated gut bacterial populations by increasing the abundance levels of Lactobacillus and Bifidobacterium, as well as reducing the abundance level of Enterobacteriaceae. The present study demonstrated that probiotic chocolate LYC and BB12 could potentially be used as alternative agents for prophylactic constipation. © 2018 Society of Chemical Industry.

Bile deficiency induces changes in intestinal Cl(-) and HCO3 (-) secretions in mice.

Biliary tract obstruction is a common clinical lesion. However, the effect of biliary tract obstruction on intestinal secretion is poorly understood. In this study, we made an investigation on intestinal HCO3 (-) and Cl(-) secretions in an experimental model of murine biliary duct ligation. Murine intestinal mucosal HCO3 (-) and Cl(-) secretions were examined in vitro in Ussing chambers by pH-stat and short-circuit current (Isc ) techniques. The mRNA and protein expressions of the cystic fibrosis transmembrane conductance regulator (CFTR) and the Na(+) -K(+) -2Cl(-) cotransporter (NKCC1) were analysed by real-time PCR, western blot and immunohistochemistry. Basal Cl(-) secretion and forskolin-stimulated duodenal and jejunal mucosal HCO3 (-) and Cl(-) secretions in mice with common biliary duct ligation were markedly elevated, compared with controls (P < 0.05 and P < 0.01). Further experiments showed that basal Cl(-) secretion and forskolin-stimulated duodenal and jejunal mucosal HCO3 (-) and Cl(-) secretions in mice with external bile drainage were also markedly elevated. CFTRinh -172 inhibited forskolin-stimulated HCO3 (-) and Cl(-) secretions. The mRNA and protein expression levels of CFTR and NKCC1 in the intestinal mucosa with both biliary duct ligation and external bile drainage were markedly higher than those in controls (P < 0.001). Bile acid administration restored the changes in function and expression of CFTR and NKCC1 in the intestinal mucosa. Bile deficiency in the intestine up-regulates the expressions of intestinal mucosal CFTR and NKCC1 and enhances intestinal mucosal HCO3 (-) and Cl(-) secretion capacity, which contributes to the understanding of intestinal physiological function for patients with biliary duct obstruction.

Pituitary adenylate cyclase-activating peptide (PACAP) immunoreactivity distribution in the small intestine of the adult New Hampshire chicken

We conducted a study in which we demonstrated by means of immunoperoxidase and immunofluorescence methods the presence of pituitary adenylate cyclase-activating peptide 38 (PACAP-38) immunoreactivity in the small intestine of adult New Hampshire chickens and its co-localization with VIP. In particular we describe for the first time the presence of PACAP-positive cells in the epithelium of crypts and villi. Using double immunostaining, we observed that these two peptides were widely co-localized in the nerve structures of duodenum and jejunum with the exception of the ileum, where we noticed a faint co-localization regarding the nerve fibers of the lamina propria of the villi. Furthermore, the two peptides were occasionally co-stored in the epithelial cells of the mucosa. Our findings suggest that in the chicken small intestine, PACAP can be considered, not only as a neuromodulator released by nerve elements, but also as a gut hormone secreted by endocrine cells, and it appears likely to have a role in the regulation of important intestinal physiological functions.

Review article: mechanisms of initiation and perpetuation of gut inflammation by stress.

Inflammatory bowel disease involves an interaction between genetic susceptibility, a host mucosal immune response and the enteric flora. However, the relapsing and remitting course underlines the importance of other modifiers, such as psychological stress. Doctors and patients share the view that stress plays a role in the initiation and perpetuation of disease. Levels of chronic perceived stress have been shown to correlate with symptom relapse and mucosal appearance, and stress management therapy has been shown to be beneficial. Animal models provide further evidence that stress may play a role in disease initiation and reactivation. Elucidation of the gut-brain-immune axis has provided insight into the mechanisms by which stress may result in gut inflammation. Stress can alter intestinal physiological function. Stress can increase gut permeability, increase ion secretion by a mechanism involving neural stimulation or mast cells, increase mucin release and deplete goblet cells. Stress causes parasympathetic activation via a mechanism involving corticotropin releasing factor, ultimately affecting mucosal mast cells. Stress also results in increased bacterial adherence and decreased luminal lactobacilli. As a result of all these changes luminal antigens may gain access to the epithelium, causing inflammation.