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At least 865 records · Page 48Linked to original sources
PubMed1993

Intestinal mast cell responses in idiopathic inflammatory bowel disease. Histamine release from human intestinal mast cells in response to gut epithelial proteins.

Mucosal and submucosal mast cell hyperplasia is a feature of the chronic inflammatory bowel diseases--ulcerative colitis and Crohn's disease. The mast cells are often seen to be degranulated in areas of active disease, suggesting that the inflammatory mediators released from these cells contribute to the pathophysiology of these disorders. We examined the hypothesis that epithelial cell-derived proteins, intestinal epithelial cell-associated components (ECAC), interact with the mast cells of patients with chronic inflammatory bowel disease to trigger the local release of mast cell mediators. Aliquots of human intestinal mucosal mast cell suspensions obtained from surgically resected specimens of colon or small intestine (ulcerative colitis, 12; Crohn's disease, 3; histologically normal controls, 8) were incubated with 1-100 micrograms/ml of colon or small bowel-derived murine ECAC or control kidney protein, or 1 microgram/ml goat anti-human IgE positive control for 30 min at 37 degrees C. Supernatants were analyzed in duplicate for histamine content by fluorometric assay. The median percent total histamine released by chronic inflammatory bowel disease mast cell suspensions to colonic epithelium-derived protein (ECAC-C) was 4% histamine (range 0-20%), such that the distribution of histamine release values in inflammatory bowel disease specimens was significantly different from the distribution of values in mast cells taken from normal mucosa (median 0%, P < 0.05). The median histamine release by all chronic inflammatory bowel disease specimens was also increased in response to the ECAC preparations derived from small bowel epithelium in that a third of the inflammatory bowel disease specimens showed greater than 10% histamine release to ECAC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Intestinal neuronal degeneration in a patient with chronic idiopathic intestinal pseudoobstruction.

Neuropathological examination of the gut in a patient with chronic idiopathic intestinal pseudoobstruction and temporal lobe epilepsy showed a degeneration of Auerbach's and of Meissner's plexus. The extent of generative changes increased in an aboral to oral direction. Neuronal degeneration was characterized by ballooning of the cytoplasm of the ganglial cells, by a hyperargyrophilia, a shortening and dilation of cell processes, and a progressive fragmentation and loss of axons. In rectal biopsies, a PAS-positive granular material was detected in the cytoplasm of ballooned ganglial cells. A severe peripheral neuropathy with fiber degeneration in the posterior columns and axonal lesions within ventral nerve roots and a more recent fiber degeneration in the lateral columns corresponding to the picture of subacute combined degeneration of the spinal cord and a symmetrical Ammon's horn sclerosis was present. This case of progressive intestinal neuronal degeneration of unknown origin is a newly described condition leading to chronic idiopathic intestinal pseudoobstruction.

Adolescent↗
PubMed1995

Accumulation of donor-specific cytotoxic T cells in intestinal lymphoid tissues following intestinal transplantation.

Utilizing a rat model of semiallogeneic intestinal transplantation, recipients were evaluated for accumulation of donor-specific cytotoxic T cells in spleen, mesenteric lymph nodes, Peyer's patches, lamina propria, and intraepithelial lymphocytes using limiting dilution analysis. Naive animals exhibited a low frequency of cytotoxic T cells in spleen and mesenteric lymph nodes with minimal activity detected in Peyer's patches and intraepithelial lymphocytes, but not detectable activity in lamina propria. Orthotopic intestinal transplantation resulted in significant increases in cytotoxic T-cell activity in recipient Peyer's patches as early as Day 6 and by Day 8 in spleen, mesenteric lymph nodes, lamina propria and intraepithelial lymphocyte populations. Graft lamina propria and intraepithelial lymphocytes exhibited significant cytotoxic T-cell activity as early as 4 days following transplant. The highest donor-specific cytotoxic T-cell activity was observed in graft intraepithelial lymphocytes on Day 8 posttransplant. These studies demonstrate rapid expansion of donor-specific cytotoxic T cells which migrate to the graft site within 4 days after semiallogeneic intestinal transplantation.

Animals↗
PubMed1996

Intestinal IgA deposition in Henoch-Schönlein purpura with severe gastro-intestinal manifestations.

UNLABELLED: In patients with Henoch-Schönlein purpura (HSP) presenting with severe gastro-intestinal (GI) symptoms, IgA deposition was studied in endoscopically obtained mucosal biopsies. A total number of 11 patients (male, 7; female, 4) were enrolled in this study; 7 patients underwent upper GI endoscopy and biopsy 1 underwent sigmoidoscopy and 3 underwent both. Upper GI endoscopy in each patient showed various mucosal changes including redness, petechiae, erosions, and ulcerations, most predominant in the second part of the duodenum. Sigmoidoscopy demonstrated no abnormality in two of four patients. Intestinal deposition of IgA was positive in 7 of 11 patients with HSP. Histological examination showed non-specific inflammation of varying degrees in each patient, but no small vessel vasculitis was observed. IgA deposits were seen in only 2 of 23 control subjects with various GI diseases. Positive rate of IgA deposition per patient was significantly higher in patients with HSP than in controls (P < 0.005). CONCLUSION: IgA deposition in the GI tract, as in the skin and kidneys, is characteristic of HSP. Intestinal IgA deposition complements the diagnostic criteria of HSP.

Child↗
PubMed1989

Early alterations of rat intestinal diamine oxidase activity by azoxymethane, an intestinal carcinogen.

Some mutagenic hydrazino compounds are also diamine oxidase inhibitors. Therefore, this interrelationship was studied for the intestinal carcinogen azoxymethane. In vitro, azoxymethane was a very weak inhibitor of rat intestinal diamine oxidase activity. In vivo, after subcutaneous injection of a single dose of azoxymethane, diamine oxidase activity was increased in the duodenum but was mainly inhibited in the colon. Intestinal diamine oxidase activity may then be influenced by regulatory processes induced by azoxymethane rather than by a direct effect.

Amine Oxidase (Copper-Containing)↗
PubMed2001

Primary localized amyloidosis of the small intestine presenting as an intestinal pseudo-obstruction: report of a case.

A 47-year-old man with primary amyloidosis confined to the small intestine is reported. Thickening of the folds and multiple polypoid protrusions were found in the duodenum by upper gastrointestinal endoscopy. Because the patient presented with a persistent intestinal pseudo-obstruction, partial jejunectomy was performed. Histological examination of the resected tissue revealed massive deposits of amyloid throughout the jejunal wall. Neither a predisposing condition nor any other sites of deposition were found, and primary amyloidosis of the small intestine was diagnosed. This rare form of amyloid deposition should be recognized so that an early diagnosis can be made.

Amyloidosis↗
PubMed2003

Down-regulation of a gastric transcription factor, Sox2, and ectopic expression of intestinal homeobox genes, Cdx1 and Cdx2: inverse correlation during progression from gastric/intestinal-mixed to complete intestinal metaplasia.

PURPOSE: The molecular mechanisms underlying the development of intestinal metaplasia (IM) of the human stomach have yet to be clarified in detail. Besides ectopic expression of intestinal transcription factors, Cdx1 and Cdx2, little information is available regarding other regulatory factors. Hence, we here analyzed Sox2, a human homolog of a chicken gastric transcription factor, with reference to our new classification for gastric/intestinal (GI)-mixed type IM. METHODS: Twenty specimens of surgically resected antral mucosa were subjected to a gland isolation technique. Isolated glands were classified into gastric (G), GI-mixed, and solely intestinal (I) types according to Alcian blue and paradoxical concanavalin A staining and were quantified for mRNA levels of gastrointestinal markers. RESULTS: MUC5AC and MUC6 transcripts decreased with the progression of IM, while MUC2 and villin-1 were inversely correlated. Sox2 showed a gradual decrease from G, through GI, to the I type (G vs GI and GI vs I, P<0.01 and P<0.005, respectively). On the other hand, Cdx1 (G vs GI and GI vs I, P<0.0001 and P=0.337, respectively) and Cdx2 (G vs GI and GI vs I, P<0.0001 and P<0.05, respectively) appeared in IM. Immunohistochemical study confirmed decreased expression of Sox2 and ectopic emergence of Cdx2 protein in IM glands. CONCLUSION: Down-regulation of Sox2, besides ectopic expression of Cdx genes, may be important factors for the development of IM.

Avian Proteins↗
PubMed1985

The synaptic relationship between vasoactive intestinal polypeptide (VIP)-like immunoreactive neurons and their axon terminals in the rat small intestine: light and electron microscopic study.

The present study demonstrates synaptic contacts between vasoactive intestinal polypeptide (VIP)-like immunoreactive neurons and immunoreactive axon terminals in the submucous and myenteric plexuses of the rat small intestine. Our observations suggest that VIP afferents directly affect the VIP neurons in the small intestine via synapses.

Animals↗
PubMed1991

Intestinal effects of the products of lipid digestion on gastric electrical activity in the cat. Possible involvement of vagal intestinal receptors sensitive to lipids.

The relationship between the lipid content of the intestinal lumen and gastric motor activity was studied in anesthetized cats. For this purpose the electromyographic activity was recorded in the antrum whereas the small intestine (duodenum and first part of jejunum or ileum) was perfused with various solutions including calcium propionate, tributyrin, sodium caprylate, potassium oleate, mixtures containing linoleic acid, monolein, triolein, mixture of triglycerides, and glycerol. Long-chain lipids and glycerol both induced a decrease in the rate of basal antral activity. This effect was found to depend on the state of lipid hydrolysis (triglycerides, monoglycerides, and fatty acids) and was most marked with monolein, linoleic acid, and glycerol. With the middle-chain lipids used, these effects were only slight; short-chain lipids did not induce any visible changes in gastric activity. All these effects were prevented by cervical bivagotomy. It was concluded that the two types of lipid-sensitive vagal receptors, which we recently showed to exist in the small intestine, trigger an inhibitory enterogastric reflex that contributes to the regulation of gastric emptying.

Animals↗
PubMed1991

A tungsten-supplemented diet delivered by transplacental and breast-feeding routes lowers intestinal xanthine oxidase activity and affords cytoprotection in ischemia-reperfusion injury to the small intestine.

Ischemia-reperfusion injury has been implicated as playing a major role in the development of necrotizing enterocolitis, a major cause of morbidity and mortality in the newborn. A tungsten-supplemented molybdenum-free diet can reduce xanthine oxidase (XO) enzyme activity in the intestine, which in turn reduces the generation of oxygen radicals after an ischemia-reperfusion insult. This study evaluated the ability of this diet to be effective by indirect means, ie, transplacental and breast-feeding routes. XO activity of the intestine was measured in three groups of CD-1 white rats: I, weanlings fed the tungsten diet or standard chow for 1 week; II, 1-day-old rat pups whose mothers were maintained on the tungsten or standard chow for 7 to 10 days prior to term; and III, rat pups at 1 and 3 weeks after birth whose lactating mothers were maintained on the tungsten or standard chow. Some animals from group III also underwent either a 30- or 60-minute episode of occlusion of the superior mesenteric artery (SMA) to evaluate the protective effects of the diet. XO activity was significantly reduced in all groups receiving the tungsten diet (P less than .0001). Blinded histopathologic studies of the entire small bowel showed significantly less villar necrosis (P less than .05) and fibrosis (P less than .0001) in the tungsten-treated group than in the controls. In the 60-minute occlusion study all tungsten-group animals survived, whereas 7 of 12 in the control group died of intestinal infarction within 24 hours (P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Differentiation and aging of the intestinal mucosa of the rat. I. Morphological, enzyme-histochemical and disc electrophoretic aspects of the prenatal and postnatal differentiation of the intestinal mucosa.

The large and small intestines of fetal, newborn, juvenile and adult rats were investigated at various points by means of enzyme histochemistry, disc electrophoretic separations of enzymes and electron microscopy. The results obtained permit division of the morphological and enzymatic differentiation of the rat intestinal epithelium into four periods of development. 1. The period of prenatal development from the 19th to the 21st fetal day with a continuous increase of the enzyme activities in the enterocytes of the entire intestinal mucosa. 2. The period of postnatal development from the first day of life until the end of the second week with enzyme activity remaining roughly the same compared with the 21st day of life. 3. The period of adaptation from the beginning of the third week of life up to the middle of the fourth week of life. During this phase the transition into the stage of adult maturity occurs both morphologically and enzymatically. 4. The stage of adult maturity, which is fully developed in the middle of the fourth week of life.

Acid Phosphatase↗
PubMed1996

Projections of neurons in the intestinal nerve of Remak to the chicken intestine.

To date, the exact site of the extrinsic postganglionic neurons innervating the intramural plexuses in the chicken intestine is unknown. In this study, neurons in the intestinal nerve of Remak (INR) were immunohistochemically labelled by injecting cholera toxin subunit B (CTb) into each one of the jejunal, ileal, cecal and rectal walls. The CTb-immunoreactive (IR) neurons were counted, and some sections from the rectal portion of INR (rectal INR) were also immunostained for either tyrosine hydroxylase (TH) or methionine enkephalin (mENK). Following injection of CTb into the jejunum or ileum, only a few CTb-IR neurons were found in the jejunal or ileal part of INR caudal to the injection site. Following injection into the more caudal intestine, CTb-IR neurons were seen in the rectal INR. Of the 3490 CTb-IR neurons that were counted in the rectal INR, 40% projected into the rostral rectum, 24% into the caudal rectum, 17% into the ileum, 10% into the cecum and only 9% into the middle rectum. Rostrocaudally dividing the rectal INR into three parts, one third of the CTb-IR neurons in the rostral part projected into the rostral rectum, the majority of CTb-IR ones in the middle part innervated the rostral rectum, and half of CTb-IR neurons in the caudal part ran into the caudal rectum. Consequently, the rostral rectum received the densest innervation, and almost all the neurons in the rectal INR exhibited an ascending projection. By double labelling, CTb-IR neurons containing TH or mENK were observed in the rectal INR after the rectal injection. The mENK-IR neurons localized in middle and caudal parts of rectal INR amounted to one third of the total CTb-IR neurons, and mainly projected into the rostral and caudal rectum. TH-and mENK-immunonegative neurons were restricted to the rostral part of rectal INR and the more rostral level.

Animals↗
PubMed2000

Decreased expression of the gut-enriched Krüppel-like factor gene in intestinal adenomas of multiple intestinal neoplasia mice and in colonic adenomas of familial adenomatous polyposis patients.

Gut-enriched Krüppel-like factor (GKLF) is a zinc finger-containing transcription factor, the expression of which is associated with growth arrest. We compared Gklf expression in intestinal and colonic adenomas to normal mucosa in multiple intestinal neoplasia (Min) mice and familial adenomatous polyposis (FAP) patients, respectively, using semi-quantitative RT-PCR. In Min mice, the level of Gklf transcript is highest in normal-appearing intestinal tissues and decreases as the size of the adenoma increases. In FAP patients, the level of GKLF transcript is lower in adenomas compared to paired normal-appearing mucosa from the same patient or normal colonic mucosa from control individuals without FAP. The possibility of DNA methylation as a cause for the decreased expression of Gklf in adenomas of Min mice was investigated by methylation-specific PCR. Results indicate that the Gklf gene is not methylated in either normal or tumorous tissues. The findings of our study are therefore consistent with the potential role of GKLF as a negative growth regulator of gut epithelial cells.

Adenoma↗
PubMed1989

Use of the peptide carrier system to improve the intestinal absorption of L-alpha-methyldopa: carrier kinetics, intestinal permeabilities, and in vitro hydrolysis of dipeptidyl derivatives of L-alpha-methyldopa.

Intestinal permeabilities of five dipeptidyl derivatives of L-alpha-methyldopa (I) were studied by an in situ intestinal perfusion method. The dipeptides displayed a significant increase in their permeabilities compared to L-alpha-methyldopa. The increases ranged from 4 to 20 times. These results suggest that the peptide transport system is less structurally specific than the amino acid transport systems and can be used as an absorption pathway for peptide analogues. The kinetic advantage demonstrated by the dipeptide, L-alpha-methyldopa-L-phenylalanine, over the amino acid analogue, L-alpha-methyldopa, suggests that the peptide carrier would be a possible route for improving the intestinal absorption of pharmacologically active amino acid analogues. Furthermore, the preliminary results of in vitro hydrolysis studies of selected dipeptidyl derivatives indicate that the peptide carrier system could be used as a base for a prodrug strategy.

Animals↗
PubMed2004

Plasma GLP-2 levels and intestinal markers in the juvenile pig during intestinal adaptation: effects of different diet regimens.

Adaptation of the residual small bowel following resection is dependent on luminal and humoral factors. We aimed to establish if circulating levels of glucagon-like peptide (GLP-2) change under different dietary regimens following resection and to determine if there is a relationship between plasma GLP-2 levels and markers of intestinal adaptation. Four-week-old piglets underwent a 75% proximal small bowel resection (n = 31) or transection (n = 14). Postoperatively they received either pig chow (n = 14), nonpolymeric (elemental) infant formula (n = 7), or polymeric infant formula alone (n = 8) or supplemented either with fiber (n = 6) or with bovine colostrum protein concentrate (CPC; n = 10) for 8 weeks until sacrifice. Plasma GLP-2 levels were measured at weeks 0, 2, 4, and 8 postoperatively. In addition, end-stage parameters were studied at week 8 including weight gain, ileal villus height, crypt depth, and disaccharidase levels. Plasma GLP-2 levels were higher in resected animals compared to transected animals fed the same diet. Plasma GLP-2 levels were significantly increased in the colostrum protein isolate-supplemented animals following resection compared to all other diet groups. The increase in plasma GLP-2 (pM) was greatest in the first 2 weeks postresection (week 0, 15.5; week 2, 30.9), followed by a plateau at weeks 2 to 4 and a decrease in GLP-2 levels from week 4 to week 8. At week 8, no relationships were found between the plasma GLP-2 levels and the measurements of weight gain, villus height, lactase, sucrase, maltase, crypt depth, or villus/crypt ratio. Plasma GLP-2 levels increase in the first weeks following massive small intestinal resection. The increase in plasma GLP-2 levels was enhanced by supplementation of the diet with CPC. The changes in GLP-2 levels observed in this study may suggest that GLP-2 plays a role in the adaptive response in the intestine following resection in this preclinical model.

Adaptation, Physiological↗
PubMed2006

Detection of pathogenic intestinal bacteria by Toll-like receptor 5 on intestinal CD11c+ lamina propria cells.

Toll-like receptors (TLRs) recognize distinct microbial components and induce innate immune responses. TLR5 is triggered by bacterial flagellin. Here we generated Tlr5-/- mice and assessed TLR5 function in vivo. Unlike other TLRs, TLR5 was not expressed on conventional dendritic cells or macrophages. In contrast, TLR5 was expressed mainly on intestinal CD11c+ lamina propria cells (LPCs). CD11c+ LPCs detected pathogenic bacteria and secreted proinflammatory cytokines in a TLR5-dependent way. However, CD11c+ LPCs do not express TLR4 and did not secrete proinflammatory cytokines after exposure to a commensal bacterium. Notably, transport of pathogenic Salmonella typhimurium from the intestinal tract to mesenteric lymph nodes was impaired in Tlr5-/- mice. These data suggest that CD11c+ LPCs, via TLR5, detect and are used by pathogenic bacteria in the intestinal lumen.

Animals↗
PubMed2002

Enhanced expression of decay-accelerating factor and CD59/homologous restriction factor 20 in intestinal metaplasia, gastric adenomas and intestinal-type gastric carcinomas but not in diffuse-type carcinomas.

AIMS: Variable expression of the complement regulatory proteins, decay-accelerating factor, CD59/homologous restriction factor 20 (HRF20) and membrane cofactor protein has been shown in human gastrointestinal malignancies, but their expression in gastric cancer has not been fully described. Thus, we immunohistochemically defined the distribution of these proteins in human normal gastric mucosa, intestinal metaplasia, adenomas and gastric cancers. METHODS AND RESULTS: Gastric tissues were obtained by endoscopic biopsy or surgical resection and stained with mouse monoclonal antibodies to decay-accelerating factor, CD59/HRF20, and membrane cofactor protein. In the normal gastric mucosa, membrane cofactor protein was diffusely stained on the basolateral surface of epithelial cells, whereas the expression of decay-accelerating factor and CD59/HRF20 was inconspicuous. In intestinal metaplasia, adenoma and intestinal-type gastric carcinoma cells, decay-accelerating factor and HRF20 were intensely stained on the apical surface; membrane cofactor protein retained its location on the basolateral surface. In diffuse-type gastric carcinomas, the expression of decay-accelerating factor, CD59/HRF20 was lost, but membrane cofactor protein was present on the tumour cell surface. CONCLUSIONS: These findings suggest that membrane cofactor protein plays a primary role in the regulation of complement activation in normal and neoplastic gastric cells and that the expression pattern of the complement regulatory proteins is closely related to gastric carcinoma development.

Adenoma↗
PubMed2006

Role of intestinal epithelial cells in the innate immune defence of the pig intestine.

The intestinal epithelium serves as a dynamic barrier, which in the course of its normal function, maintains regulated uptake of nutrients and water while excluding potential pathogens. Over the past decade many studies have also revealed the immunological importance of intestinal epithelial cells (IEC). IEC have developed a variety of mechanisms to reduce the risk of infection by invasive pathogens or damage by toxic compounds. The effective maintenance of a physical barrier function is dependent on the establishment of well-organised intercellular junctions and a constant state of regeneration/renewal of the epithelium. IEC also participate in the innate immune responsiveness of the intestine by their ability to secrete mucus and antimicrobial peptides. IEC are also able to secrete cytokines and to respond to exogenous chemokines. This review summarises the current knowledge of the innate immune mechanisms developed by porcine IEC.

Animals↗