Lumen Of Small Intestine Research Articles

L-Glutamine or l-alanyl-l-glutamine prevents oxidant- or endotoxin-induced death of neonatal enterocytes

This study tested the hypothesis that L-glutamine (Gln) or L-alanyl-L-glutamine (Ala-Gln) prevents oxidant- or endotoxin-induced death of neonatal enterocytes. Enterocytes of neonatal pigs rapidly hydrolyzed Ala-Gln and utilized Gln. To determine whether Gln or Ala-Gln has a cytoprotective effect, IPEC-1 cells were cultured for 24 h in Gln-free Dulbecco's modified Eagle's-F12 Ham medium containing 0, 0.5, 2.0 or 5.0 mM Gln or Ala-Gln, and 0, 0.5 mM H(2)O(2) or 30 ng/ml lipopolysaccharide (LPS). Without Gln or Ala-Gln, H(2)O(2)- or LPS-treated cells exhibited almost complete death. Gln or Ala-Gln at 0.5, 2 and 5 mM dose-dependently reduced H(2)O(2)- or LPS-induced cell death by 14, 54 and 95%, respectively, whereas D: -glutamine, alanine, glutamate, ornithine, proline, glucosamine or nucleosides had no effect. To evaluate the effectiveness of Gln or Ala-Gln in vivo, 7-day-old piglets received one-week oral administration of Gln or Ala-Gln (3.42 mmol/kg body weight) twice daily and then a single intraperitoneal injection of LPS (0.1 mg/kg body weight); piglets were euthanized in 24 and 48 h to analyze intestinal apoptotic proteins and morphology. Administration of Gln or Ala-Gln to LPS-challenged piglets increased Gln concentrations in small-intestinal lumen and plasma, reduced intestinal expression of Toll-like receptor-4, active caspase-3 and NFkB, ameliorated intestinal injury, decreased rectal temperature, and enhanced growth performance. These results demonstrate a protective effect of Gln or Ala-Gln against H(2)O(2)- or LPS-induced enterocyte death. The findings support addition of Gln or Ala-Gln to current Gln-free pediatric amino acid solutions to prevent intestinal oxidative injury and inflammatory disease in neonates.

The effect of ulinastation on the small intestine injury and mast cell degranulation in a rat model of sepsis induced by CLP

Introduction Sepsis could be initiated by the gastrointestinal tract injury and subsequent bacterial translocation. In the present experiment, we aimed to investigate effect of ulinastatin (UTI) on the small intestinal injury and bacterial translocation in septic rats and role of mast cells degranulation in its action. Methods Fifty-four male Wistar rats were randomly divided into three groups: sham laparatomy, cecal ligation and punture (CLP), and CLP plus UTI. CLP was used to develop septic rat model and UTI was administered to rats intraperitoneally (50,000 U/kg) 30 min prior to CLP operation. After CLP or sham operation, variable parameters were investigated in three subsets of animals. One subset was used for measurements of nitrite and nitrate (NO x ) concentration in plasma at 1, 6, 12, 18, and 24 h and levels of NO x and iNOS mRNA in the small intestine, RMCP-II released into the small intestinal lumen, bacterial translocation and morphologic changes at 24 h. The other subsets were used for the small intestinal motility and microvascular in vivo at 24 h. Results Bacterial translocation, barrier injury, impaired motility and blood flow, mast cells degranulation of the small intestine in the CLP group were found more severe than that in the sham group. Elevated RMCP-II, NO x , and iNOS mRNA levels were also detected in the CLP group. Application of UTI not only protected the small intestine from sepsis but also diminished changes of intestinal mast cells. Conclusion UTI can significantly ameliorate the small intestinal injury and subsequent bacterial translocation by inhibiting mast cells degranulation in septic rats.

Phytates reduce uptake of leucine and glutamate but not lysine and glucose from the intestinal lumen of chickens: Short communication

An investigation into the influence of phytates on the in situ absorption of amino acids (lysine, glutamate and leucine) and glucose from the intestinal lumen of 3-week-old chickens was carried out. Birds were anaesthetised and the intestines exteriorised. Uptake of 5 mM of each nutrient over a 4-min period was measured in the presence of four phytate concentrations (0, 50, 250 and 500 mM). Five birds were used for each nutrient at each concentration of phytate tested. Leucine uptake decreased linearly (P < 0.001) and that of glutamate showed a tendency to decrease (P = 0.055) as the phytate concentration increased. Absorption of lysine and glucose were unaffected by the presence of phytate. In conclusion, phytate in the small intestinal lumen exerted a depressive effect on the absorption of specific free amino acids from the lumen. Its depressive effect was greatest for leucine followed by glutamate, and phytate had little effect on the absorption of lysine.

En bloc combined liver and small-bowel transplantation in rats: construction of a cuff in portal vein

Objective To establish a model of en bloc combined liver/small bowel transplanta-tion in the rat. Methods Homoplastic transplantation of en bloc combined liver and small-bowel in Wistar rats was performed. As for the donor operation, the portal vein and superior mesenteric artery were flushed with 4℃ cold Ringer's solution. The small intestinal lumen was flushed with 4℃ cold Ne-omycin solution. The donor small bowel and liver were harvested, preserved and transplanted as a whole. The donor inferior vena eava in abdomen was cut to construct a muff in the lateral wall of por-tal vein and cuff was placed. For the recipient operation, the orthotopie liver transplantation was com-pleted at first by using Kamada's two cuff technique, and then the donor abdominal aorta was anasto-mosed end to side to the receptor abdominal aorta artery to set up superior mesenteric artery and prop-er hepatic artery blood flow under a microscope. The lower ileum was exteriorized as stoma in right lower abdomen. Results The successful rate of operation was 86 %. The mean survival time of the grafted rats was over 30 d. The transplanted liver and small bowel were normal in histology. Conclu-sion It is feasible to establish a model of en bloc combined liver and small bowel transplantation by constructing a cuff in portal vein. Key words: Liver transplantation; Liver; Small bowel; Rat

Effects of 2-hydroxy-4-methylthiobutyrate on portal plasma flow and net portal appearance of amino acids in piglets

To determine whether portal plasma flow (PPF) and net portal appearance of amino acids (AA) could be affected by 2-hydroxy-4-methylthiobutyrate (HMB), six barrows (35-day-old, 8.6+/-1.4 kg), implanted with arterial, portal and mesenteric catheters, were fed a DL-methionine (as the control) or HMB-supplemented diet once hourly and infused intramesenterically with 1% p-amino hippurate. PPF was numerically 9% higher (P=0.09) in HMB-fed pigs than in controls over a 4-6 h period. Compared with controls, pigs fed the HMB diet had increased (P<0.05) net portal balance and/or appearance of leucine, isoleucine, histidine, arginine and alanine, but had decreased (P<0.05) portal appearance of glutamate over a 6-h period. The concentration of acetate in the lumen of the distal small intestine was higher (P=0.01) in HMB-fed pigs than in controls (25.14 vs. 7.64 mmol/kg). mRNA levels for proglucagon and endothelial nitric-oxide synthase (eNOS) in stomach and proximal small intestine, and mRNA levels for GLP-2 receptor (GLP-2R) in stomach were higher (P<0.05) in HMB-fed pigs compared with those in controls. Collectively, HMB supplementation increased concentrations of short-chain fatty acids in intestinal lumen, expression of proglucagon, GLP-2R, and eNOS genes, and net portal absorption of AA. These novel findings from the study with pigs may also have important implications for intestinal nutrition and health in humans.

Enterocyte chloride and water secretion into the small intestine after enterotoxin challenge: Unifying hypothesis or intellectual dead end?

Many forms of diarrhoeal disease, particularly so called "secretory" diarrhoeal disease are thought to arise by the active secretion of chloride ion from the enterocytes, creating an osmotic gradient for fluid movement into the small intestinal lumen. This model implies that normally occurring intestinal secretion is catastrophically enhanced by bacterial enterotoxins. This review advocates that neither normal nor abnormal intestinal secretion from the enterocytes occurs and that no competent proof for chloride secretion exists. Prior to 1970, the physiological evidence failed to support the concept of the formation of intestinal juice as a normal intestinal event. The concept was later revived to explain the high rate of fluid entry into the lumen after exposure to cholera toxin. Much evidence has been advanced for the chloride secretion hypothesis, the dominant secretory paradigm after 1974, but is the evidence sufficiently compelling for it to be regarded as proving the chloride secretory model? The evidence falls into four categories and a fifth conjectural argument that proposes that an abnormal chloride ion channel in cystic fibrotic sufferers confers a natural selective advantage by preventing diarrhoeal disease. Secretion is putatively demonstrated by 1) showing that mass transfer of fluid is into the lumen (secretion) and not merely a failure to transport out of the lumen (failed absorption). Support is offered by 2) chloride ion flux measurements in vitro in Ussing chambers and by 3) short-circuit current measurements that are consistent with and purport to show chloride ion movement into the lumen. In addition, 4) pharmacological agents are identified that affect short-circuit current and these are assumed to be anti-secretory, consistent with the biochemical mechanism for secretion, confirmed wherever possible by mouse knock-out models. Finally, the proxy methods used to study water movement such as elevated short-circuit current measurements show these to be absent in cystic fibrotic patients. The enterocyte secretion hypothesis is challenged here on the basis of an examination of the methods used to show secretion, particularly after exposing the small intestine to heat stable enterotoxin (STa) from E. coli. STa is thought to be secretory because fluid entry into the lumen is claimed, enhanced isotopic flux of chloride ion towards the lumen occurs, an increase in short-circuit current is found, preventable by various drugs that are deemed likely to be anti-secretory and also because the short-circuit current changes after STa are not seen in cystic fibrotic patients. Using volume recovery in vivo, STa is found not to be secretory but only anti-absorptive. Hence, other techniques used to show secretion are not fit for that purpose. If STa is identified as secretory and yet no secretion occurs, how reliable is the evidence for other toxins being secretory when these methods are used? This review concludes that chloride ion secretion is unproven. A review of the literature indicates that secretion occurs not because epithelial cells actively pump water but by interdiction of fluid absorption, increased conductivity through tight junctions and an increased hydrostatic driving force through elevated capillary pressure. The exclusive focus on chloride secretion may explain the failure to develop antisecretory drugs over the last three decades.

Release of metabolic enzymes by Giardia in response to interaction with intestinal epithelial cells

Giardia lamblia, an important cause of diarrheal disease, resides in the small intestinal lumen in close apposition to epithelial cells. Since the disease mechanisms underlying giardiasis are poorly understood, elucidating the specific interactions of the parasite with the host epithelium is likely to provide clues to understanding the pathogenesis. Here we tested the hypothesis that contact of Giardia lamblia with intestinal epithelial cells might lead to release of specific proteins. Using established co-culture models, intestinal ligated loops and a proteomics approach, we identified three G. lamblia proteins (arginine deiminase, ornithine carbamoyl transferase and enolase), previously recognized as immunodominant antigens during acute giardiasis. Release was stimulated by cell–cell interactions, since only small amounts of arginine deiminase and enolase were detected in the medium after culturing of G. lamblia alone. The secreted G. lamblia proteins were localized to the cytoplasm and the inside of the plasma membrane of trophozoites. Furthermore, in vitro studies with recombinant arginine deiminase showed that the secreted Giardia proteins can disable host innate immune factors such as nitric oxide production. These results indicate that contact of Giardia with epithelial cells triggers metabolic enzyme release, which might facilitate effective colonization of the human small intestine.

Micromolar concentration of kynurenic acid in rat small intestine

Kynurenic acid is an antagonist of glutamate and alpha-7 nicotinic acetylcholine receptors and an agonist of the G: -protein-coupled receptor GPR35, which is predominantly expressed in immune and gastrointestinal tissues. In this study, we report that kynurenic acid is present in the lumen of rat small intestine in micromolar concentration sufficient to affect the GPR35 receptor. Moreover, we show that kynurenic acid can be produced by Escherichia coli. We suggest that kynurenic acid may modulate gastrointestinal function and integrity.

A Case of Multiple Intussusceptions in the Small Intestine Caused by Metastatic Renal Cell Carcinoma

Renal cell carcinoma (RCC) may metastasize to almost any organ, but metastasis to the small bowel is rare. Small bowel metastasis from RCC can induce obstruction or bleeding, and perforation can also be induced in rare case. Yet RCC metastasis to the small bowel is unlikely to be a direct cause of intussusceptions. A few cases of intussusceptions caused by small intestinal metastasis of RCC have been reported, but multiple small intestinal intussusceptions are extremely rare. We report here on a 47-year-old male patient who presented to the emergency room with acute abdominal pain. He had undergone radical nephrectomy 2 years previously due to left RCC. The abdominal CT scan revealed enhanced masses with the "target" sign that suggested enteric intussusceptions in the jejunum. Eight pedunculated masses within the small intestinal lumen led to intussusceptions at 30 and 150 cm distal to Treitz ligament. Three segmental resections of the small intestine and functional end to end anastomosis were done. The patient recovered uneventfully from this operation. To the best of our knowledge, this is the 1(st) report of metastases from RCC that presented as synchronous intraluminal polypoid tumors, and these tumors served as the lead points for two intussusceptions in the jejunum.

In this issue

In this issue

MyD88-mediated signals induce the bactericidal lectin RegIIIγ and protect mice against intestinal Listeria monocytogenes infection

Listeria monocytogenes is a food-borne bacterial pathogen that causes systemic infection by traversing the intestinal mucosa. Although MyD88-mediated signals are essential for defense against systemic L. monocytogenes infection, the role of Toll-like receptor and MyD88 signaling in intestinal immunity against this pathogen has not been defined. We show that clearance of L. monocytogenes from the lumen of the distal small intestine is impaired in MyD88−/− mice. The distal ileum of wild-type (wt) mice expresses high levels of RegIIIγ, which is a bactericidal lectin that is secreted into the bowel lumen, whereas RegIIIγ expression in MyD88−/− mice is nearly undetectable. In vivo depletion of RegIIIγ from the small intestine of wt mice diminishes killing of luminal L. monocytogenes, whereas reconstitution of MyD88-deficient mice with recombinant RegIIIγ enhances intestinal bacterial clearance. Experiments with bone marrow chimeric mice reveal that MyD88-mediated signals in nonhematopoietic cells induce RegIIIγ expression in the small intestine, thereby enhancing bacterial killing. Our findings support a model of MyD88-mediated epithelial conditioning that protects the intestinal mucosa against bacterial invasion by inducing RegIIIγ.

Yersinia enterocolitica Infection of Mice Reveals Clonal Invasion and Abscess Formation

Yersinia enterocolitica is a common cause of food-borne gastrointestinal disease leading to self-limiting diarrhea and mesenteric lymphadenitis. Occasionally, focal abscess formation in the livers and spleens of certain predisposed patients (those with iron overload states such as hemochromatosis) is observed. In the mouse oral infection model, yersiniae produce a similar disease involving the replication of yersiniae in the small intestine, the invasion of Peyer's patches, and dissemination to the liver and spleen. In these tissues and organs, yersiniae are known to replicate predominantly extracellularly and to form microcolonies. By infecting mice orally with a mixture of equal amounts of green- and red-fluorescing yersiniae (yersiniae expressing green or red fluorescent protein), we were able to show for the first time that yersiniae produce exclusively monoclonal microcolonies in Peyer's patches, the liver, and the spleen, indicating that a single bacterium is sufficient to induce microcolony and microabscess formation in vivo. Furthermore, we present evidence for the clonal invasion of Peyer's patches from the small intestine. The finding that only very few yersiniae are required to establish microcolonies in Peyer's patches is due to both Yersinia-specific and host-specific factors. We demonstrate that yersiniae growing in the small intestinal lumen show strongly reduced levels of invasin, the most important factor for the early invasion of Peyer's patches. Furthermore, we show that the host severely restricts sequential microcolony formation in previously infected Peyer's patches.

Involvement of UDP-glucuronosyltransferase activity in irinotecan-induced delayed-onset diarrhea in rats

We assessed the involvement of UDP-glucuronosyltransferase (UGT) activity in episodes of irinotecan hydrochloride (CPT-11)-induced delayed-onset diarrhea using a mutant rat strain with an inherited deficiency of UGT1A (Gunn rats). Gunn rats exhibited severe diarrhea after the intravenous administration of CPT-11 at a dose of 20 mg/kg, whereas Wistar rats did not. In the epithelium of the small intestine and cecum in Gunn rats, the shortening of villi, degeneration of crypts, and destruction of the nucleus were observed. The AUC, MRT, and t (1/2) of CPT-11, and the AUC of 7-ethyl-10-hydroxycamptothecin (SN-38) in plasma were, respectively, 1.6-fold, 1.5-fold, 1.7-fold, and 6.5-fold higher, and the cumulative biliary excretion rate of SN-38 was 2.3-fold higher, in Gunn rats than Wistar rats. SN-38 glucuronide excreted via bile in Wistar rats was not de-conjugated in the small intestinal lumen. The SN-38 AUC values in small intestinal tissues were also 5.0 to 5.8-fold higher in Gunn rats than Wistar rats. In conclusion, Gunn rats developed severe delayed-onset diarrhea after i.v. administration of CPT-11 at a much lower dose. Severe intestinal impairments would be induced in Gunn rats through exposure to SN-38 at high levels for a long period mainly via the intestinal lumen and partially via the bloodstream. These results clarified that the deficiency of UGT activity contributed greatly to the induction of the CPT-11-induced delayed-onset diarrhea and epithelial impairment in the intestine. In the clinic, great care is needed when using chemotherapy with CPT-11 in patients with poor UGT activity.

Soybean Phosphatidylcholine-Induced Enhancement of Lymphatic Absorption of Triglyceride Depends on Chylomicron Formation in Rats

We investigated whether chylomicron formation is involved in the dietary phosphatidylcholine (PC)-induced increase in triglyceride (TG) absorption using an inhibitor of chylomicron formation, pluronic L-81 (L-81). In rats, cannulas were implanted into the duodenum (exps. 1 and 2) and the mesenteric lymph duct (exp. 1), and an emulsified lipid solution containing the test lipids (soybean oil, SO or soybean oil plus phosphatidylcholine, LE) with or without L-81 was infused through a duodenal cannula at a rate 3 ml/h for 2 h, and followed by infusion of a glucose-NaCl solution for 2 h. Mesenteric lymph was collected for 4 h (exp. 1). In exp. 2, the mucosa and contents of the small intestine were collected at 20, 40, or 90 min after the start of duodenal infusion of the test lipid to evaluate accumulation of lipids incorporated into the mucosa in the rats without a lymph cannula. In exp. 1, lymphatic TG outputs rapidly increased with infusion of both test lipids without L-81, but L-81 abolished these increases. TG accumulated in the small intestinal mucosa with L-81 treatment in a time-dependent manner, but the levels of accumulation were similar between the SO and LE groups (exp. 2). There were no differences in the amounts of lipid remaining in the small intestinal lumen between the L-81-treated SO and LE groups. These results indicate that uptake of lipid into the mucosal cells was not increased by LE. We conclude that the formation of chylomicron is responsible for increases in the promotive effect of a high level of dietary PC on the lymphatic absorption of TG.

Nippostrongylus brasiliensis: Reversibility of reduced-energy status associated with the course of expulsion from the small intestine in rats

Gastrointestinal nematodes require energy for active establishment in the gut against intestinal flow and peristaltic motion. In this study we employed CellTiter-Glo ® Luminescent Cell Viability Assay to measure the ATP value of individual adult Nippostrongylus brasiliensis during the course of immune-mediated expulsion from the small intestine in rats. The ATP values of adult worms taken from the lumen of the distal small intestine were lower than worms collected from the lumen of the proximal small intestine. Moreover, values from worms in the lumen of the proximal small intestine were lower than those from worms in the mucosa, the preferred site of adult N. brasiliensis. The reduction of ATP values in worms from each region was observed not only at expulsion phase, but also at established phases of the infection suggesting that energy metabolism of the parasites is independent of host immune response. When adult worms with low ATP values on day 12 post-infection were implanted surgically into the small intestine of naïve rats, the worms re-established in recipients and completely restored the ATP values. Short in vitro culture of adult worms under low oxygen tension resulted in low ATP value in the worms. These results suggested that adult worms were dislodged from their preferred site by intact energy metabolism activity.

Role of iNOS‐derived nitric oxide (NO) on hind limb ischemia/reperfusion (I/R)‐induced remote injury to the gut

Systemic inflammatory response syndrome (SIRS), as a consequence of ischemia/reperfusion (I/R) negatively influences the function of the affected organs. In this study we assessed the potential mechanisms (role of NO) of remote intestinal inflammatory response elicited by hind limb I/R. To this end C57BL/6 (WT) and iNOS−/− mice were subjected to 1h of bilateral hind limb ischemia followed by 6h of reperfusion. Some WT mice were injected (s.c.) with iNOS inhibitor, 1400W (5mg/kg) immediately before induction of ischemia. The obtained results indicate that hind limb I/R results in dysfunction of the gut as assessed by the increase in total protein levels (Bradford assay), TNF-a protein (ELISA) and NO (Griess reaction) in the lumen of small intestine. In addition, hind limb I/R results in an increase in leukocyte accumulation (intravital microscopy and MPO assay), TNF-a and iNOS protein expression (Western blots) in the mucosa of small intestine. Important to note, that the most profound changes with respect to the gut dysfunction were found in jejunum and ileum, whereas duodenum was affected the least. Interfering with iNOS activity (1400W and iNOS−/− mice) significantly attenuated hind limb I/R-induced leukocyte recruitment to the gut mucosa and dysfunction of the small intestine. Taken together these data indicate that hind limb I/R induces remote inflammatory response in the small intestine through iNOS-derived NO dependent mechanism (HSFO-NA5580 and MOP-68848)

EXPRESSION OF PANETH CELL ANTIMICROBIAL PEPTIDES IN RESPONSE TO HELICOBACTER HEPATICUS INFECTION.

Purpose Paneth cells are important regulators of host-microbe interactions at mucosal surfaces, playing a key role in innate immunity by secreting antimicrobial peptides into the small intestinal lumen. Some pathogenic bacteria have developed virulence mechanisms that have allowed them to inhibit expression and/or function of these antimicrobial peptides. Helicobacter hepaticus , a mammalian pathogen, localizes to the cecum and intestinal crypts. H. hepaticus possesses a cytolethal distending toxin (CDT), which modulates the host immune system and is essential for long-term intestinal colonization. Therefore, we set about determining whether H. hepaticus might down-regulate the expression of Paneth cell antimicrobials as one of its virulence mechanisms during infection, thereby facilitating H. hepaticus colonization. Methods Samples of distal small intestine obtained 2 weeks after bacterial inoculation were analyzed from three groups of mice: uninfected wild-type C57BL/6 mice, mice infected with H. hepaticus , and mice infected with an isogenic H. hepaticus CDT mutant. Quantitative real-time PCR was performed using external standards to determine the absolute values of mRNA levels of 21 target genes, which included mouse Paneth cell antimicrobial peptides, other Paneth cell products, cytokines, and other intestinal antimicrobials. The data were analyzed using Student9s t -test. Results In mice infected with H. hepaticus , the cytokines KC (a human interleukin-8 equivalent) and tumor necrosis factor α (TNF-α) showed significant increases in expression when compared with levels in uninfected mice, consistent with mucosal inflammation in the infected samples. Other genes showed no changes in expression levels when comparing uninfected wild-type mice to mice infected with H. hepaticus . Little or no effect was seen on the expression of any tested genes with infection of the isogenic H. hepaticus CDT mutant. Conclusion Our data do not support the hypothesis that H. hepaticus infection down-regulates expression of Paneth cell products. There is evidence that H. hepaticus infection stimulates changes in the host defense response, specifically, increasing expression of the cytokines KC and TNF-α. The mechanism(s) by which H. hepaticus evades the innate immune defense mechanisms of Paneth cells remains a topic for further study.

Mucosal immunomodulation by the non-bacterial fraction of milk fermented by Lactobacillus helveticus R389

The health promoting effects ascribed to probiotic bacteria and fermented dairy products arise not only from bacteria themselves but also from metabolites derived from milk fermentation. Exopolysaccharides produced during milk fermentation and peptides derived from major milk proteins, when released during fermentation, are potential modulators of various regulatory processes in the body. The aim of this work was to increase the knowledge of the previously observed immunomodulating capacity of milk fermented by Lactobacillus helveticus R389 by the study of the mucosal immunomodulation exerted by the non-bacterial fraction of the milk fermented at a constant pH6 (NBFpH6). The effects on IL-6 production by small intestine epithelial cells, the profile of IgA+ and cytokine+ cells (IL-2, IL-6, IL-10, TNF-α and IFN-γ) induced in the gut lamina propria, and the levels of total and specific secretory IgA in the lumen of BALB/c mice that received NBFpH6 for 2, 5 or 7 days were examined. There was an increase in the number of IgA+, IL-10+, IL-2+ and IL-6+ cells after all feeding periods. Total S-IgA in the small intestine lumen increased in mice that received NBFpH6 for 2 days. However, no specific antibodies against NBFpH6 were detected. Feeding of NBFpH6 for 7 days significantly ( P < 0.05) enhanced IL-6 secretion by small intestine epithelial cells. NBFpH6 induced a non-specific mucosal response that was down-regulated for protective immunity, enhancing IL-6 production by epithelial cells and IgA production in the small intestine. These events improve the immunological defenses at the intestinal level, increasing host protection against pathologies. Because mucosal immune responses induced by certain dietary antigens play a large part in the prevention of gastrointestinal diseases, the oral administration of a mucosal adjuvant such as NBFpH6 may positively affect the milieu of the intestinal lumen. The opportunity exists then to manipulate the constituents of the lumen of the intestine through dietary means, thereby enhancing the health condition of the host.

Video Capsule Endoscopy: Clinical Relevance of Capsule Endoscopy Findings

Video capsule endoscopy (VCE) is a novel diagnostic tool for noninvasively visualizing the lumen of the entire small intestine. It is especially useful in identifying the source of obscure small intestinal bleeding. However, VCE is not always optimal for localizing small bowel lesions. Several studies show VCE to be markedly superior to standard diagnostic techniques although the true clinical relevance of many of the capsule endoscopic findings remain unknown. We present two case reports of VCE findings that resulted in surgical intervention but were found to be benign lesions on definitive pathological examination. The actual clinical relevance of many of the lesions found on VCE thus remains to be demonstrated.

Green tea catechins inhibit pancreatic phospholipase A 2 and intestinal absorption of lipids in ovariectomized rats

This study was conducted to examine whether the inhibition of intestinal lipid absorption by green tea is associated with the inhibitory effect of its catechins on pancreatic phospholipase A 2 (PLA 2). PLA 2 activity was assayed by using 1,2-dioleoylphosphatidylcholine (DOPC), porcine pancreatic PLA 2 and catechins at varying concentrations (0.075–1.80 μmol/L). The amount of 1-oleoyl-2-hydroxyphosphatidylcholine liberated was determined by HPLC. The percentage of inhibition of PLA 2 by catechins at 0.6 μmol increased in the order of (−)-epicatechin (23.3%), (+)-catechin (CAT; 24.8%), (−)-epigallocatechin (25.7%), (−)-epicatechin gallate (39.7%) and (−)-epigallocatechin gallate (EGCG; 64.9%). In an in vivo study, ovariectomized rats with lymph cannula were infused intraduodenally for 8 h with a triolein emulsion containing [dioleoyl-1- 14C]-phosphatidylcholine, DOPC, α-tocopherol (αTOH) and retinol (ROH) without (CAT0) or with CAT or EGCG. The lymphatic total 14C-radioactivity was significantly lowered by EGCG (45.5±4.9% dose) compared with CAT (56.2±5.2% dose) and CAT0 (64.7±2.0% dose). The 14C-radioactivity remaining in the small intestinal lumen and cecum was higher in EGCG (24.1% dose) than in CAT (9.5% dose) and CAT0 rats (9.0% dose). Significantly less 14C radioactivity was incorporated into lymph triacylglycerol and cholesteryl ester in EGCG rats. The absorption of αTOH, used as a marker of extremely hydrophobic lipids, was significantly lower in EGCG (7.8±1.7 μmol) than in CAT (14.4±2.8 μmol) and CAT0 rats (16.8±2.1 μmol). The absorption of ROH was unaffected, whereas oleic acid output was lower in EGCG rats. The results show that EGCG inhibits the intestinal absorption of lipids, which is in part associated with its inhibition of phosphatidylcholine hydrolysis. Data suggest that EGCG may inhibit the absorption of other highly lipophilic organic compounds.