The phytonutrient cinnamaldehyde limits intestinal inflammation and enteric parasite infection.

Phytonutrients such as cinnamaldehyde (CA) have been studied for their effects on metabolic diseases, but their influence on mucosal inflammation and immunity to enteric infection are not well documented. Here, we show that consumption of CA in mice significantly down-regulates transcriptional pathways connected to inflammation in the small intestine, and alters T-cell populations in mesenteric lymph nodes. During infection with the enteric helminth Heligomosomoides polygyrus, CA treatment attenuated infection-induced changes in biological pathways connected to cell cycle and mitotic activity, and tended to reduce worm burdens. Mechanistically, CA did not appear to exert activity through a prebiotic effect, as CA treatment did not significantly change the composition of the gut microbiota. Instead, in vitro experiments showed that CA directly induced xenobiotic metabolizing pathways in intestinal epithelial cells and suppressed endotoxin-induced inflammatory responses in macrophages. Collectively, our results show that CA down-regulates inflammatory pathways in the intestinal mucosa and can limit the pathological response to enteric infection. These properties appear to be largely independent of the gut microbiota, and instead connected to the ability of CA to induce antioxidant pathways in intestinal cells. Our results encourage further investigation into the use of CA and related phytonutrients as functional food components to promote intestinal health in humans and animals.

Localization of Claudin-3 and Claudin-4 within the Small Intestine of newborn piglets.

Piglets must acquire passive immunity through colostrum within hours after birth to survive. How colostral macromolecules traverse the small intestinal epithelium may include nonselective pinocytosis and paracellular transport through tight junction proteins located between epithelial cells. Claudin proteins-3 and -4 contribute to the epithelial tight junctions (TJs) on the apical aspect of lateral surfaces of intestinal epithelial cells (IECs) where they help regulate ion and macromolecule movement across the intestinal epithelium. Throughout the small intestine of newborn piglets, Claudin-3 was localized to the lateral and basolateral surface of intestinal epithelial cells as well as the membrane of large vacuoles. In the duodenum and jejunum, Claudin-4 was localized to the apical surface independent of tight junction regions. In the ileum, Claudin-4 was localized to the lateral and basolateral surfaces indicating region-specific differences and noncanonical patterns of Claudin-4 localization independent of tight junction regions. Understanding the timing of changes in surface localization of Claudin-3 and Claudin-4 and how they may coincide with changes in small intestinal permeability may help develop new protective strategies against infectious diseases within newborn piglets.

Effect of Acrylamide Supplementation on the Population of Vasoactive Intestinal Peptide (VIP)-Like Immunoreactive Neurons in the Porcine Small Intestine.

Acrylamide is one of the harmful substances present in food. The present study aimed to establish the effect of acrylamide supplementation in tolerable daily intake (TDI) dose (0.5 µg/kg b.w./day) and a dose ten times higher than TDI (5 µg/kg b.w./day) on the population of vasoactive intestinal peptide-like immunoreactive (VIP-LI) neurons in the porcine small intestine and the degree of the co-localization of VIP with other neuroactive substances (neuronal nitric oxide synthase (nNOS), substance P (SP), and cocaine- and amphetamine-regulated transcript peptide (CART)). In our work, 15 Danish landrace gilts (5 in each experimental group) received capsules (empty or with low or high doses of acrylamide) for a period of 28 days with their morning feeding. Using double immunofluorescence staining, we established that acrylamide supplementation increased the number of neurons showing immunoreactivity towards VIP in all types of enteric nervous system (ENS) plexuses and fragments of the small intestine studied. Moreover, both doses of acrylamide led to changes in the degree of co-localization of VIP with nNOS, SP, and CART in intramural neurons. The observed changes may be the adaptation of neurons to local inflammation, oxidative stress, or the direct toxic effects of acrylamide on intestinal neurons, also referred to as neuronal plasticity.

Immunomodulatory activity and protective effects of chokeberry fruit extract on Listeria monocytogenes infection in mice.

Chokeberry (Aronia melanocarpa) fruit extracts (CE) are rich in polyphenols and usually exhibit immunomodulatory, anti-viral and anti-bacterial effects. We have previously shown that the CE used in this study activated macrophages and stimulated effector T cell differentiation in vitro. When applied orally to healthy mice, CE increased the proportion of CD11c+ dendritic cells in the gut-associated lymphoid tissue. CE-pretreated BALB/c mice readily eradicated orally ingested Listeria monocytogenes as evidenced by a slighter decrease in body weight and number of bacteria recovered from the spleen and reduced spleen size compared to the control infected mice. CE pretreatment in infected mice resulted in higher proportions of CD11b+ macrophages and CD8+ cytotoxic T cells both in the gut and the spleen. Phagocytosis, reactive oxygen species production and the proportions of activated CD86+ macrophages (CD11b+) and dendritic cells (CD11c+) were also enhanced in CE-pretreated infected mice. Furthermore, the expression of inducible nitric oxide synthase and IL-6 was increased in CE-pretreated infected mice and similar results were obtained in peritoneal macrophages in vitro. This effect of CE was associated with increased phosphorylation of IκB and Notch1 production. Finally, CE pretreatment elevated the proportion of perforin-producing cells in the spleen compared to control infected mice. This study demonstrates that prophylactic treatment with CE leads to more rapid eradication of bacterial infection with L. monocytogenes predominantly through increased activity of myeloid cells in the gut and in the spleen.

Protective Effect of Tong-Qiao-Huo-Xue Decoction on Inflammatory Injury Caused by Intestinal Microbial Disorders in Stroke Rats.

Tong-Qiao-Huo-Xue Decoction (TQHXD) is a classic traditional Chinese medicine prescription for treating cerebral ischemia. The purpose of this study was to investigate the effect of TQHXD on intervening inflammatory response of ischemic stroke by regulating intestinal flora and repairing the intestinal barrier. A rat model of cerebral ischemia was established using middle cerebral artery occlusion (MCAO) and behavioral scores were performed. Additionally, the high throughput 16S ribosomal DNA (rDNA) sequence of intestinal bacteria in fecal samples of rat was also carried out. Our results showed that TQHXD could change the main components of intestinal flora in stroke rats, and reduced the excessive increase of Bacteroidetes, and also regulated the abnormal changes of abundance of some flora as well. In addition, the intestinal epithelial barrier was damaged after stroke, allowing bacterial metabolites to enter the blood, while TQHXD had an improved effect on this phenomenon. Meanwhile, pathological changes in the brain tissue and infarct volume were also alleviated by TQHXD. Due to the disorder of the intestinal flora and the destruction of the barrier, the peripheral immune imbalance caused an inflammatory reaction. TQHXD improved the imbalance of T cells, and inhibited the inflammatory response. Finally, the therapeutic transplantation of fecal microbiota also improved the outcome of stroke in rats. Our presented results suggest that TQHXD may improve the gut microbiota disorder and its induced inflammatory response after stroke, which could be a new target and mechanism for the treatment of stroke.

A multicomponent mycotoxin deactivator modifies the response of the jejunal mucosal and cecal bacterial community to deoxynivalenol contaminated feed and oral lipopolysaccharide challenge in chickens1.

Mycotoxin deactivators are a widely used strategy to abrogate negative effects of mycotoxin-contaminated feed. It has not been adequately evaluated whether these deactivators may detoxify bacterial toxins in the intestinal lumen and subsequently lower the inflammatory response in chickens. The present objective was to study the effect of a multicomponent mycotoxin deactivator (B), containing a bentonite and a bacterial strain capable to enzymatically biotransform trichothecenes especially deoxynivalenol (DON), when supplemented to a DON-contaminated feed in combination with an oral lipopolysaccharide challenge on visceral organ size, expression of innate immune genes and mucosal permeability in the small intestine as well as on the cecal bacterial composition and metabolites in broiler chickens. Eighty 1-d-old male chickens were randomly allotted to four treatment groups in two replicate batches (n = 10/treatment/replicate): 1) basal diet without DON (CON), 2) CON diet supplemented with B (2.5 mg B/kg feed) (CON-B), 3) CON diet contaminated with 10 mg DON/kg feed (DON), and 4) DON diet supplemented with 2.5 mg B/kg feed (DON-B). In half of the chickens per treatment, effects were assessed under nonchallenge conditions, whereas in the other half of birds, to increase their intestinal bacterial toxin load, effects were tested after an oral challenge with 1 mg LPS/kg BW from Escherichia coli O55:B5 on the day before sampling. DON reduced (P < 0.05) the weight of bursa fabricii and thymus. DON increased the expression level of intestinal alkaline phosphatase at the duodenal mucosa (P = 0.027) but did not modify jejunal gene expression and mucosal permeability. The LPS challenge decreased the jejunal MUC2 expression but increased ZO1 and IL6 expression compared to the unchallenged animals (P < 0.05). DON × B interactions indicated lower expression of IL10 in duodenum and NFKB in jejunum with the B diet but higher expression with the DON-B diet (P = 0.050). Furthermore, the B lowered jejunal expression of NFKB and IL6 but only in LPS-challenged chickens (P < 0.05). Alterations in the cecal microbiota composition and VFA profile were likely associated with alterations in host physiology in the small intestine caused by DON, B, and LPS. According to the present data, B appeared to have potential to detoxify antigens other than DON in the intestinal lumen of chickens, whereby the toxin load may limit the efficacy of B to modify the intestinal and systemic response as indicated by interactions of DON, B, and LPS.

Dose-dependent effects of two inulin types differing in chain length on the small intestinal morphology, contractility and proinflammatory cytokine gene expression in piglets.

Inulin is a linear fructose polymer which may affect small intestinal physiology. The effects of dietary level of two inulin types on morphology, contractility and proinflammatory cytokine gene expression in the small intestine of piglets were investigated. Fifty six piglets were divided into seven groups fed diets without inulin addition or with 1%, 2% or 3% of inulin with an average degree of polymerisation of 10 (IN10) or 23 (IN23). All diets were offered from day 10 of life for 40 d. Feeding IN10 diets did not affect villous height to crypt depth ratio in the duodenum, while in the jejunum the 2% IN10 diet increased it as compared to other groups. Jejunal muscle contractions induced by electrical field stimulation were impaired by the 2% and 3% IN10 diets. The ileal expression of interleukin-12p40 was decreased by the 2% IN10 diet. There was no effect of IN23 level on villous height to crypt depth ratio in any segment of the small intestine as well as on jejunal motility. The 2% and 3% IN23 diets decreased the jejunal expression of tumour necrosis factor-α. In conclusion, IN10 is more active in the small intestine than IN23. At the 2% dietary level, it increases absorptive area in the jejunum, but may slightly impair smooth muscle contractions.

Melatonin alleviates oxidative stress in sleep deprived mice: Involvement of small intestinal mucosa injury.

BACKGROUND: Previous research demonstrated that sleep deprivation (SD) resulted in intestinal homeostasis disorder in colon. The present study was further performed to clarify the role of melatonin in SD-induced small intestinal (SI) mucosal injury. METHODS: We successfully established a multiplatform 72 h SD mouse model with or without melatonin supplementation to explore the improvement of melatonin in the destruction of SI induced by SD. RESULTS: Melatonin supplementation suppressed an increase of corticosterone level and a decrease of melatonin level caused by SD. Meanwhile, we observed that melatonin supplementation in sleep deprived mice markedly reversed a decrease of the villi length/crypt depth (V/C) ratio and the number of goblet cells, PCNA positive cells, the expressions of MUC2 and tight junction proteins, as well as an upregulation of the expressions of autophagic proteins in the duodenum, jejunum and ileum. Furthermore, melatonin supplementation inverted the SD-induced the decline of antioxidant enzyme activities (T-AOC and CAT etc) and anti-inflammatory cytokines (IL-10 and IFN-γ) and the increase of oxidative product MDA, pro-inflammatory cytokines (IL-6 and TNF-α), p-P65 and p-IκB proteins in the SI. CONCLUSIONS: These findings suggested that melatonin may be used as a probiotic agent to reverse SD-induced SI mucosa injury by suppressing oxidative stress and NF-κB pathway activation.

Leptin and EGF Supplementation Enhance the Immune System Maturation in Preterm Suckling Rats.

In preterm newborns the immaturity of the immune system is remarkable, with reduced innate and adaptive immune responses. Many bioactive compounds in breast milk, such as growth factors and adipokines, contribute to the immune system's maturation in early life. However, studies on the immunoregulatory activity in preterm neonates are practically nonexistent. The aim of the present study was to determine whether a nutritional supplementation in early life with leptin or epidermal growth factor (EGF) was able to promote the maturation of the systemic and intestinal immune system in preterm conditions. For this purpose, premature rats were daily supplemented by oral gavage with leptin or EGF. Term and Preterm groups receiving vehicle were used as controls. Preterm rats showed deficiencies compared to full-term ones, such as lower body weights, erythrocyte counts, plasma IgG and IgM concentrations and B cell percentages, and higher values of Th and Tc TCRαß+ cells in mesenteric lymph nodes, and intestinal permeability, among others. However, leptin and EGF supplementation were able to revert some of these deficiencies and to improve the premature immune system's development. These results suggest that leptin and EGF are involved in enhancing the maturation of the systemic and intestinal immune system in preterm conditions.

Dietary addition of Artemisia argyi reduces diarrhea and modulates the gut immune function without affecting growth performances of rabbits after weaning1.

The present study was conducted to investigate the effect of Artemisia argyi on the production performance and intestinal barrier of rabbits. Weaned Hyla rabbits (30 d, n = 160) of similar body weight were divided into 4 groups (40 rabbits per treatment), and they were fed a control diet or fed an experimental diet supplemented with 3%, 6%, or 9% A. argyi. The results showed that the dietary supplementation with A. argyi did not affect the rabbits' food intake and body weight gain regardless of the inclusion level but decreased the diarrhea rate and diarrhea index (P < 0.05). Dietary addition of A. argyi increased the small intestine length and villus height/crypt depth, regardless of the inclusion level (P < 0.05). Compared with the control, the A. argyi supplementation increased the gene expression of zonula occludens 1 (ZO-1) and claudin 1 in all segments of the small intestine and regardless of the level of A. argyi (P < 0.05). In the duodenum, a dietary supplementation with 6% and 9% A. argyi increased the immunoglobulins A (IgA) content (P < 0.05). In the jejunum, the A. argyi supplementation decreased interleukin 2 (IL2) and IL6 content regardless of the inclusion level (P < 0.05). In the ileum, a 3% A. argyi addition decreased IL2 content, whereas a 6% A. argyi addition decreased IL6 content (P < 0.05). Furthermore, 6%-9% A. argyi supplementation increased the IgA content in the ileum (P < 0.05). In conclusion, dietary addition of A. argyi reduces diarrhea and modulates the gut immune function without affecting growth performances of rabbits.

Hesperidin Effects on Gut Microbiota and Gut-Associated Lymphoid Tissue in Healthy Rats.

Hesperidin, found in citrus fruits, has shown a wide range of biological properties. Nonetheless, a more in-depth investigation is required on the effects on the immune system, and in particular, on the gut-associated lymphoid tissue, together with its relationship with the gut microbiota. Therefore, we aimed to establish the influence of oral hesperidin administration on the intestinal lymphoid tissue and on the gut microbiota composition in healthy animals. Lewis rats were orally administrated 100 or 200 mg/kg hesperidin three times per week for four weeks. Microbiota composition and IgA-coated bacteria were determined in caecal content. Mesenteric lymph node lymphocyte (MLNL) composition and functionality were assessed. IgA, cytokines, and gene expression in the small intestine were quantified. Hesperidin administration resulted in a higher number of bacteria and IgA-coated bacteria, with changes in microbiota composition such as higher Lactobacillus proportion. Hesperidin was also able to increase the small intestine IgA content. These changes in the small intestine were accompanied by a decrease in interferon-γ and monocyte chemotactic protein-1 concentration. In addition, hesperidin increased the relative proportion of TCRαß+ lymphocytes in MLNL. These results show the immunomodulatory actions of hesperidin on the gut-associated lymphoid tissue and reinforce its role as a prebiotic.

Attenuating effect of melatonin on lipopolysaccharide-induced chicken small intestine inflammation.

Enriched melatonin (MEL) has been found in the mammalian intestine and has been recently demonstrated to alleviate rodent colitis. In this study, the effect of MEL on lipopolysaccharide (LPS)-induced intestinal inflammations was investigated in new chicken hatchlings. The chicks were fed with a diet supplemented with MEL (12.5 mg/day) from D1 to D10. Meanwhile, the chicks in the LPS or MEL + LPS groups were injected with LPS (10 mg/kg BW, i.p.) at D10. LPS treatment for 6 h increased the expression of IL-6, IL-4, caspase-3 mRNAs and TUNEL-positive cell populations, but decreased populations of the goblet and PCNA+ cells, IgA production and the expression of MUC2 mRNA in the duodenum. Compared with the LPS group, MEL pre-feeding alleviated duodenal inflammation and decreased the expression of TNF-α mRNAs by 23.6% (P = 0.004), IL-6 mRNAs by 69.4% (P = 0.001), IL-4 mRNAs by 4.1% (P = 0.824) and caspase-3 mRNAs by 45.8% (P < 0.001). Conversely, MEL pre-feeding attenuated the LPS-induced changes of IgA production by 161.6% (P = 0.013) and PCNA+ cell populations by 172.1% (P < 0.001) in the duodenum. TLR4 mRNA was also up-regulated by LPS treatment but down-regulated by MEL pre-feeding. In conclusion, dietary MEL could attenuate LPS-induced chick duodenal inflammation by down-regulating the expression of inflammatory cytokines, promoting epithelial cell proliferation, improving the immunological barrier and inhibiting epithelial apoptosis via the mediation of TLR4.

Cellular Composition of the B- and T-Cell-Dependent Areas in the Small Intestine during the Post-Stress Period (Experimental Study).

A quantitative study of lymphoid cells in the B- and T-cell-dependent areas of intestinal lymphoid nodules and mesenteric lymph nodes in behaviorally passive and active rats was performed at various periods after acute stress on the model of 1-h immobilization with simultaneous electrocutaneous stimulation. Stress exposure is accompanied by a decrease in the number of lymphoid cells in immunogenic structures of the gastrointestinal tract. Post-stress changes in the cytoarchitectonics of B- and T-cell-dependent areas in mesenteric lymph nodes of animals are less pronounced than in lymphoid nodules. Quantitative changes in lymphoid cells of B-cell-dependent areas in the small intestine of rats are greater than in T-cell-dependent areas. Changes in the cellular composition of immunogenic structures in the digestive system are most significant at the early stages of the post-stress period (1st week). Passive rats are characterized by significant changes in the cytoarchitectonics of B- and Tcell-dependent areas in the small intestine after extreme exposure, which illustrates functional exhaustion of the lymphoid tissue in stress-predisposed specimens.

Polysaccharides derived from Ganoderma lucidum fungus mycelia ameliorate indomethacin-induced small intestinal injury via induction of GM-CSF from macrophages.

Non-steroidal anti-inflammatory drugs often cause ulcers in the human small intestine, but few effective agents exist to treat such injury. Ganoderma lucidum Karst, also known as "Reishi" or "Lingzhi", is a mushroom. We previously reported that a water-soluble extract from G. lucidum fungus mycelia (MAK) has anti-inflammatory effects in murine colitis induced by trinitrobenzene sulfonic acid, and induction of granulocyte macrophage colony-stimulating factor (GM-CSF) by MAK may provide anti-inflammatory effects. However, its effects on indomethacin-induced small intestinal injuries are unknown. The present study investigated the preventative effects of MAK via immunological function and the polysaccharides from MAK on indomethacin-induced ileitis in mice. Peritoneal macrophages (PMs) were stimulated in vitro with MAK and adoptively transferred to C57BL/6 mice intraperitoneally, which were then given indomethacin. Intestinal inflammation was evaluated after 24h. We performed in vivo antibody blockade to investigate the preventive role of GM-CSF, which derived from PMs stimulated with MAK. We then used PMs stimulated with MAK pre-treated by pectinase in an adoptive transfer assay to determine the preventive role of polysaccharides. Indomethacin-induced small intestinal injury was inhibited by adoptive transfer of PMs stimulated in vitro with MAK. In this transfer model, pre-treatment with anti-GM-CSF antibody but not with control antibody reversed the improvement of small intestinal inflammation by indomethacin. Pectinase pretreatment impaired the anti-inflammatory effect of MAK. PMs stimulated by MAK appear to contribute to the anti-inflammatory response through GM-CSF in small intestinal injury induced by indomethacin. The polysaccharides may be the components that elicit the anti-inflammatory effect.

Sodium butyrate ameliorates S100/FCA-induced autoimmune hepatitis through regulation of intestinal tight junction and toll-like receptor 4 signaling pathway.

BACKGROUND AND AIM: Recent investigation revealed that dysbiosis in the gut flora and disruption of permeability of intestinal barrier are possible causes for the development of autoimmune hepatitis. Supplementation of sodium butyrate has been suggested to protect liver injury from disrupted permeability of small intestine. In current study, we employed S100/Freund's complete adjuvant induced autoimmune hepatitis to investigate therapeutic efficacy of sodium butyrate and its mechanism in the liver and upper small intestine. METHODS: C57BL/6 mice were employed and divided into three groups - control group (n=8), autoimmune hepatitis group (n=12) and autoimmune hepatitis with treatment of sodium butyrate group (n=12). Histological staining and western blot analyses were employed to evaluate liver and upper small intestine morphology and gene expression respectively. RESULTS: The findings revealed that S100/Freund's complete adjuvant caused liver injury and disruption of upper small intestine villi. Sodium butyrate attenuated the injuries and prevented migration of Escherichia coli into the liver. Moreover, the effect of sodium butyrate on protection of injuries of the liver and upper small intestine could be due to inhibition of toll-like receptor 4 signaling pathway, as well as its down-regulation of inflammatory cytokines - interleukin-6 and tumor necrosis factor-a. CONCLUSIONS: Sodium butyrate can prevent liver injury by maintaining the integrity of small intestine and inhibiting inflammatory response in S100/Freund's complete adjuvant induced autoimmune hepatitis.

Effects of early enteral nutrition supplemented with collagen peptides on post-burn inflammatory responses in a mouse model.

The effect of early enteral nutrition (EN) supplemented with Alaska pollock skin-derived collagen peptides (CPs) on post-burn inflammatory responses was investigated in a mouse model. Male blab/c mice were randomly assigned to four groups: a sham burn (SB) group, a control group (burn + EN + glycine, BE), a positive control group (burn + EN + glutamine, BEG) and a treatment group (burn + EN + CPs, BEC). Burn-induced increases of serum endotoxin level, and systemic and intestinal concentration of TNF-α and IL-6 were attenuated in BEG and BEC at post-burn day (PBD) 1, 3 and 7 (p < 0.05 vs. BE). Notably, BEC revealed a prominent decrease of the serum endotoxin level, TNF-α and IL-6 as compared to BEG at PBD 7 (p < 0.05). Furthermore, EN supplemented with CPs diminished the phosphorylation of intestinal NF-κB p65 and simultaneously down-regulated the mRNA expression of TNF-α and IL-6 in small intestine (p < 0.05 vs. BE). Also, it demonstrated a comparable effect with glutamine in ameliorating post-burn inflammatory responses in mice with burns. Therefore, CPs could be considered as a potential immunonutrient supplement in EN to improve post-burn outcomes in burn patients.

Chronic diarrhea associated with high serum level of immunoglobulin A and diffuse infiltration of plasma cell in small intestine: A case report.

RATIONALE: Chronic diarrhea in adult patients due to various causes is very common in clinic, but patient suffering with mal-absorption due to immunoproliferative small intestinal disease was rarely reported in China. PATIENT CONCERNS AND DIAGNOSES: A 35-year-old female presented with more than three years history of chronic diarrhea, rickets, high serum value of immunoglobulin A protein, and anemia. Bone marrow aspiration suggested that the patient was in a sideropenic and megalobastic anemia stage. Duodenal and ileac biopsies revealed atrophy and blunting villi. The bowel lamina propria was infiltrated with slightly increased intraepithelial lymphocytes and mainly with diffuse plasma cells. The following enzyme labeling immunohistochemistry results were strongly positive to alpha-heavy-chain. Computed tomography manifested she had diffuse thickening of small intestine wall. At last a diagnosis of immunoproliferative small intestinal disease was made. INTERVENTIONS AND OUTCOMES: On the first month, the patient was treated with vitamin D supplements, calcium, magnesium, potassium, iron, folic acid, mecobalamin replacements and microflora probiotics. The patient frequency of water diarrhea alleviated slightly, but her weight loss, anxiety neurosis and other disorders were still severe. After taking with prednisone (40 mg per day, and gradually reduced to the lowest dose) for another month, the symptoms was gradually subsided. LESSONS: The study shows that immunohistochemical staining for alpha-heavy chain proteins should be completed on small intestine biopsy specimens if the patient is suspected a diagnosis of immunoproliferative small intestinal disease.

Electroacupuncture treatment partly promotes the recovery time of postoperative ileus by activating the vagus nerve but not regulating local inflammation.

Postoperative ileus (POI) after abdominal surgery significantly lowers the life quality of patients and increase hospital costs. However, few treatment strategies have successfully shortened the duration of POI. Electroacupuncture (EA) is a modern way of administering acupuncture and widely used in various gastrointestinal (GI) diseases in the world. Here, we studied the effect of EA on POI and its underlying mechanisms. Intestinal manipulation resulted in significant delays of GI transit, colonic transit and gastric emptying. Surgery also up-regulated c-fos in nucleus of the solitary tract (NTS) and induced inflammation response in the small intestine. Further, operation and inhale anesthesia inhibited NTS neuron excitation duration for the whole observation time. EA administered at ST36 indeed shortened the recovery time of GI and colonic transit, and significantly increased the gastric emptying. EA also significantly activated the NTS neurons after operation. However, there was no anti-inflammation effect of EA during the whole experiment. Finally, atropine blocked the regulatory effect of EA on GI function, when it was injected after surgery, but not before surgery. Thus, the regulatory effect of EA on POI was mainly mediated by exciting NTS neurons to improve the GI tract transit function but not by activating cholinergic anti-inflammatory pathway.

Ganoderma lucidum beta 1,3/1,6 glucan as an immunomodulator in inflammation induced by a high-cholesterol diet.

BACKGROUND: Binding of beta 1,3/1,6 glucan of Ganoderma lucidum (G. lucidum) with the receptor results in a series of signal transfers (signalling cascades), which activates the transcription factors for regulating inflammation. Excess cholesterol intake leads to an increase in the distance between fat cells and capillaries, which may cause hypoxia in the fat tissue of obese mice. This hypoxia induces the death of fat cells, resulting in the inflammation of adipose tissue or an increase in the inflammatory gene expression associated with obesity. METHODS: The current study examined the immunomodulation effect of G. lucidum beta 1,3/1,6 glucan according to immunoglobulin, poly-Ig receptor expression, Nature Killer cell (NK cell) activity, lymphocytes proliferation and cytokines expression. RESULTS: Our present study shows that feeding G. lucidum beta 1,3/1,6 glucan to mice induces IgA or IgG expression in the serum and small intestine washing fluid and enhances poly-Ig receptor expression in the small intestine moreover, the observation of the IL-2 and Nature killer cell activity were exchanged. CONCLUSIONS: The effect of a high-cholesterol diet in the inflammatory response was observed in heart, liver, kidney, spleen, and colon tissues through histopathological evaluations. The presented evidence demonstrates that the inflammation response in the high-cholesterol diet group was much higher than in the other groups and the beta 1,3/1,6 glucan reduces inflammation in obese mice fed a high-cholesterol diet.

Prebiotic inulin supplementation modulates the immune response and restores gut morphology in Giardia duodenalis-infected malnourished mice.

Malnutrition induces a state of growth retardation and immunologic depression, enhancing the host susceptibility to various infections. In the present study, it was observed that prebiotic supplementation either prior or simultaneously with Giardia infection in malnourished mice significantly reduced the severity of giardiasis and increased the body and small intestine mass, along with increased lactobacilli counts in faeces compared with malnourished-Giardia-infected mice. More specifically, prebiotic supplementation significantly increased the levels of anti-giardial IgG and IgA antibodies and anti-inflammatory cytokines IL-6 and IL-10 and reduced the pro-inflammatory cytokine TNF-α, along with increased levels of nitric oxide in both the serum and intestinal fluid of malnourished-prebiotic-Giardia-infected mice compared with malnourished-Giardia-infected mice. Histopathology and scanning electron microscopy of the small intestine also revealed less cellular and mucosal damage in the microvilli of prebiotic-supplemented malnourished-Giardia-infected mice compared with severely damaged mummified and blunted villi of malnourished-Giardia-infected mice. This is the first study to report that prebiotic supplementation modulated the gut morphology and improved the immune status even in malnourished-Giardia-infected mice.