PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “INTESTINAL MUCOSA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources

Human intestinal mucosa alters T-cell reactivities.

BACKGROUND: Compared with T cells in peripheral blood, lamina propria T lymphocytes have a low proliferative response to stimulation via the T-cell antigen receptor/CD3 complex or by protein kinase C activators yet largely preserve or even show an enhanced reactivity to CD2 and CD28 triggering. Coculture of peripheral blood T lymphocytes with intestinal mucosa supernatant leads to a similar functional behavior as found in freshly recovered lamina propria T lymphocytes. The aim of this study is to characterize the nature of substances in the mucosal supernatant responsible for downregulation of T-cell receptor-dependent signals. METHODS: Mucosal supernatant was produced, dialyzed, digested with proteinase K, reduced by 2-mercaptoethanol or dithiothreitol, and tested for its activity on peripheral blood T lymphocytes. RESULTS: Supernatant lost its activity after dialysis through a membrane (pore size 12,000-14,000). Digestion with proteinase K does not abolish its activity suggesting that the substances are neither proteins nor peptides. However, its effects on T lymphocyte proliferation can be reversed by reducing agents like 2-mercaptoethanol or dithiothreitol, suggesting that oxidative substances are contained in mucosal supernatants. CONCLUSIONS: Our data support the view that mucosal substances that down-regulate antigen receptor-induced T lymphocyte proliferation are small, nonprotein, nonpeptide molecules with oxidative properties.

Antigens, Differentiation, T-Lymphocyte↗

Immunoreactivity for interleukin 3 and 5 and granulocyte/macrophage colony-stimulating factor of intestinal mucosa in bronchial asthma.

T lymphocytes and eosinophils are important components of the inflammatory cell infiltrate in bronchial mucosa in asthma. Because activated lymphocytes migrate through the thoracic duct and the general circulation to remote glandular and mucosal sites, we initiated this study to evaluate pathological abnormalities and immunoreactivity for interleukin (IL) 3, IL-5, and granulocyte/macrophage colony-stimulating factor (GM-CSF) of intestinal mucosa in bronchial asthma. 15 asthmatic patients, 8 nonasthmatic patients with chronic obstructive pulmonary disease, 6 atopic nonasthmatic healthy controls, and 6 nonatopic healthy controls were studied. Duodenal biopsies were performed by endoscopy. A significantly increased number of intraepithelial lymphocytes and eosinophils and a significant accumulation of mononuclear cells (lymphocytes and mast cells) and eosinophils in the lamina propria were detected in asthmatics and atopic controls. Immunostaining with antibodies directed against IL-3, IL-5, and GM-CSF was positive in asthmatics and atopic controls, whereas no staining was observed in nonatopic controls and chronic obstructive pulmonary disease. Combined ultrastructural study and immunogold labeling demonstrated that IL-3, IL-5, and GM-CSF were localized in eosinophils and mast cells. Although devoid of gastrointestinal symptoms, asthmatics and asymptomatic atopics had duodenal pathological abnormalities mimicking those observed in the bronchial mucosa in asthma, suggesting that the whole mucosal immune system is involved in bronchial asthma.

Adolescent↗

Small-intestinal mucosa in pseudoobstruction syndromes.

The purpose of this investigation was to determine the frequency and severity of small intestinal mucosal damage in pseudoobstruction syndromes. One hundred eighty-nine interpretable biopsies from 12 patients were blindly reviewed by two investigators. The underlying disorders were scleroderma in 7 and idiopathic intestinal pseudoobstruction in 5. All 12 had small-intestinal dilatation on small-bowel series. Eight of the 12 patients had biopsies characterized by moderate to severe mucosal damage; 3 of these had some biopsies which were flat. The damage did not correlate with: (1) types and numbers of organisms recovered from small intestinal aspirates; (2) duration of illness; (3) degree of dilatation of the proximal small bowel; (4) concentrations of deconjugated bile salts in small intestinal fluid; or (5) amount of fat absorbed in fat-balance studies. We conclude that mucosal damage is common in pseudoobstruction syndromes. The pathogenesis of the damage and its relationship to intraluminal bacteria remain undefined.

Adolescent↗

Small intestinal mucosa changes, including epithelial cell proliferative activity, of children receiving total parenteral nutrition (TPN).

We examined the small intestinal histology disaccharidase activities as well as the incorporation of [3H]thymidine into DNA of biopsies maintained in organ culture from seven children (ages 9 months to 5 years) receiving total parenteral nutrition (TPN). Three children suffered from inflammatory bowel disease and received TPN for one month (short term). Four required long-term TPN (> 9 months) for short-bowel syndrome. DNA was extracted from the samples following serial precipitation with perchloric acid. Results were compared to those from 22 age-matched children investigated for abdominal pain or chronic diarrhea. Short-term TPN resulted in slightly lower lactase, sucrase, and palatinase activities that were not statistically different from controls. Long-term TPN resulted in focal mild villus atrophy and a decrease in disaccharidase activity in two patients. Biopsies from long-term TPN patients incorporated less thymidine compared to those of controls (P < 0.001) when data was expressed per total biopsy (3.6 +/- 1.1 vs. 8.4 +/- 1.1 fmol) or per milligram of tissue (1.0 +/- 0.12 vs 2.7 +/- 0.7 fmol). The above data are in general agreement with the hypoplastic effect of TPN in animals. However, in children, much longer periods of TPN are required to realize the changes.

Adolescent↗

Lateral intercellular space volume as a determinant of CFTR-mediated anion secretion across small intestinal mucosa.

Studies of full-thickness, small intestinal preparations have shown that maximal anion secretion [indexed by short-circuit current (I(sc))] during intracellular cAMP (cAMP(i)) stimulation is transient and followed by a decline toward baseline. Declining I(sc) is preceded by decreases in transepithelial conductance (G(t)), which in the small intestine reflects the lateral intercellular space (LIS) volume of the paracellular pathway. We hypothesized that decreases in LIS volume limit the magnitude and duration of cAMP(i)-stimulated anion secretion. Experimental manipulations to increase the patency of the LIS (assessed by G(t) and electron microscopy) were investigated for an effect on the magnitude of cAMP(i)-stimulated anion secretion (assessed by the I(sc) and isotopic fluxes) across murine small intestine. In control studies, changes of G(t) after cAMP(i) stimulation were associated with a morphological "collapse" of the LIS, which did not occur in intestine of CFTR-null mice. Removal of the outer intestinal musculature, exposure to a serosal hypertonic solution, or increased serosal hydrostatic pressure minimized reductions in G(t) and increased the cAMP(i)-stimulated I(sc) response. Increased I(sc) primarily resulted from increased Cl(-) secretion that was largely bumetanide sensitive. However, bumetanide-insensitive I(sc) was also increased, and similar increases occurred in the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1)-null intestine, indicating that activities of non-NKCC1 anion uptake proteins are also affected by LIS volume. Thus LIS patency is an important determinant of the magnitude and duration of CFTR-mediated anion secretion in murine small intestine. Decreases in LIS volume may limit the pool of available anions to basolateral transporters involved in transepithelial secretion.

Animals↗

Pored domes in the capillary endothelial cells of teleost (Prochilodus scrofa) intestinal mucosa.

The mucosal capillaries of the proximal intestine in a freshwater teleost (Prochilodus scrofa) are lined by an endothelial sheet with several fenestrated or pored domes, which are observed both in the thinner and thicker cytoplasmic extensions of the endothelium. These domes sometimes communicate between the inner and the outer side of the capillary wall, forming a transendothelial channel-like structure with internal diaphragms. The pored domes seem to be a frequent structure in fishes. Their ultrastructure in the proximal segment of the intestine, where the flow of substances through the endothelium is intense, is described.

Animals↗

Apolipoprotein C-II deficiency: detection of immunoreactive apolipoprotein C-II in the intestinal mucosa of two patients.

Recent data suggest that mutant immunoreactive forms of apolipoprotein C-II (apoC-II) can be detected in the plasma of patients with the apoC-II deficiency syndrome. We studied the possible presence of apoC-II mutants in the plasma of two patients with apoC-II deficiency by immunological means. The patients were hypertriglyceridemic, and apoC-II was undetectable in plasma as determined by radial immunodiffusion, electroimmunoassay, and immunonephelometry. Furthermore, apoC-II was undetectable either by electrophoresis or by immunoblotting in the plasma of the probands, while apoC-II was present in the plasma of their parents, although at less than half-normal concentration. Immunochemical localization of apoC-II, however, showed that the apoprotein could be detected within the enterocytes obtained from the intestinal mucosa of the patients. From these data we conclude that the patients synthesize apoC-II, at least in the intestine.

Apolipoprotein C-II↗

Effects of wheat bran on the exocrine pancreas and the small intestinal mucosa in the dog.

Five Beagle dogs, equipped with duodenal and gastric fistulae, were fed a standard diet before receiving the same diet supplemented with wheat bran for 1 month. Pancreatic secretory investigations performed in conscious animals before and 1 month after bran administration showed a significant parallel increase in the flow rate of pancreatic secretion and the outputs of bicarbonate and amylase both in basal and secretin-stimulated conditions. The outputs of protein and chymotrypsin increased only in unstimulated secretions, while the output of lipase was strongly reduced in response to secretin. However, the small intestinal mucosa was not affected by bran administration. Dietary fiber did not alter the height of the villi or the activity of sucrase, maltase and aminopeptidase in mucosal homogenates or isolated brush border membranes from intestinal biopsies. These data suggest that wheat bran supplemented to the standard diet affects the exocrine pancreatic secretion but not intestinal enzyme activities involved in the absorption of carbohydrates and proteins in the dog.

Amylases↗

Differential distribution of phenol and catechol sulphotransferases in human liver and intestinal mucosa.

Phenol and catechol sulphotransferases were studied with p-nitrophenol and dopamine as substrates in the mucosa of the ileum and colon obtained from 6 subjects and also in the liver from 6 subjects. The ileum and colon were from the same donor. The kinetics of phenol and catechol sulphotransferases were studied in each tissue specimen. The maximum velocity of reaction (Vmax) for phenol sulphotransferase (in pmol X min-1 X mg-1; mean +/- SD) was 165 +/- 28 (ileum), 79 +/- 42 (colon) and 1,361 +/- 370 (liver), whereas Vmax for catechol sulphotransferase was 489 +/- 75 (ileum), 198 +/- 93 (colon) and 39 +/- 23 (liver). Phenol sulphotransferase is the predominant pathway in the liver, whereas catechol sulphotransferase is the predominant pathway in the intestine. The ileum catalysed the sulphation of p-nitrophenol and dopamine at a higher rate than the colon. The Michaelis-Menten constant (Km) for phenol sulphotransferase (in mumol/l; mean +/- SD) was 0.96 +/- 0.11 (ileum), 1.00 +/- 0.19 (colon) and 0.84 +/- 0.07 (liver), whereas Km for catechol sulphotransferase was 17.8 +/- 2.8 (ileum), 18.2 +/- 3.4 (colon) and 21.4 +/- 1.2 (liver). Km values of hepatic phenol or catechol sulphotransferases are not different from those of intestinal enzymes. Previous work has shown that 2-naphthol sulphotransferase obeys non-Michaelis-Menten kinetics in the human intestinal mucosa [Pharmacology, 1988;43:411]. Here, we show that 2-naphthol is sulphated by at least two enzymes in human intestine.

Aged↗

[Vitamin B1 resorption. IV. Level of sulfhydryl groups in intestinal mucosa resorption of 35S-thiamine].

Studies have been carried on with the aim of investigating the effect of SH-groups on the absorption of 35S-thiamine in chicken's duodenum. The trial has been performed in chickens aged 56 days; as SH-groups releasing agents L-cysteine and SH-glutathion have been utilized; urea has been used in order to release SH-groups from protein molecules. The absorption of 35S-thiamine in duodenum is significantly increased in the presence of L-cysteine, SH-glutathion and urea. 35S-thiamine appears to be stored in the intestinal mucosa more conspicuously in the presence of urea. Concomitanly with the high levels of SH-groups in the duodenal mucosa, also the thiamine absorption results to be increased (P less than 0.001).

Animals↗

Lipoprotein synthesis and secretion by cultured human intestinal mucosa.

We tested whether cultured human jejunal mucosa incorporates fatty acid into esterified lipids and whether organ culture can serve as a model system to study lipoprotein secretion by the human gut. Jejunal biopsies obtained from seven subjects were cultured for 24 h in medium containing 2 microCi of [3H]palmitic acid. More than 95% of the radioactivity incorporated by the tissue was found to be associated with esterified lipids: triglycerides, cholesterol esters and phospholipids, 7 . 8 +/- 1 . 2, 0 . 5 +/- 0 . 1 and 14 . 0 +/- 1 . 5 nmol/10 mg weight respectively. During the culture labelled triglycerides, phospholipids and cholesterol esters were secreted to the medium. Most of the newly synthesized esterified lipids in the medium were found in the d < 1 . 019 g/ml and d = 1 . 019--1 . 063 g/ml fractions. The majority of the newly synthesized triglycerides were found in the d < 1 . 019 g/ml fraction. Labelled cholesterol esters were enriched in the d = 1 . 063--1 . 21 g/ml fraction. Boiled biopsies adsorbed negligible amounts of radioactive palmitic acid and did not synthesize esterified lipids. The addition of puromycin to the culture medium and preincubation with colchicine resulted in decreased uptake of the labelled fatty acid and decreased secretion of esterified lipids to the medium. These experiments indicate that cultured human intestinal mucosa is a suitable model to study lipid synthesis and lipoprotein secretion by the human intestine.

Adolescent↗

Molecular basis of the interaction of Salmonella with the intestinal mucosa.

Salmonella is one of the most extensively characterized bacterial pathogens and is a leading cause of bacterial gastroenteritis. Despite this, we are only just beginning to understand at a molecular level how Salmonella interacts with its mammalian hosts to cause disease. Studies during the past decade on the genetic basis of virulence of Salmonella have significantly advanced our understanding of the molecular basis of the host-pathogen interaction, yet many questions remain. In this review, we focus on the interaction of enterocolitis-causing salmonellae with the intestinal mucosa, since this is the initiating step for most infections caused by Salmonella. Animal and in vitro cell culture models for the interaction of these bacteria with the intestinal epithelium are reviewed, along with the bacterial genes that are thought to affect this interaction. Lastly, recent studies on the response of epithelial cells to Salmonella infection and how this might promote diarrhea are discussed.

Animals↗

[Lactase deficiency in the intestinal mucosa. Demonstration by hydrogen detection in the expired air after lactose loading (author's transl)].

Lactose malabsorption can be demonstrated by detecting hydrogen (H2) in the expired air after oral loading with lactose. A comparative study was carried out on 24 subjects. Following an oral loading dose of lactose, the H2 eliminated during expiration was assayed by gas chromatography, and blood galactose levels were measured. The results showed that the test was reliable, well tolerated and reproductible. However, the method does not measure the amounts of lactase present in the intestinal mucosa. The lactose loading test seems to be valuable for studies on lactose and carbohydrate malabsorption.

Adult↗

[The condition of the intestinal mucosa of the proximal digestive tract subjected sectioning of the jejunal wall].

The balance between secretion and degradation of the mucosa glycoproteins in the dog intestine is preserved with the aid of local reflexes in both serous-muscular and mucous-submucous layers of the wall. Irrespective of major alterations in the glycoproteins synthesis in the mucosa, protective properties of the submucous layer are maintained owing to a high content of acetylneuraminic acid and low level of mucous glycoproteins degradation.

Animals↗

The effect of treatment on lymphokine-secreting cells in the intestinal mucosa of children with Crohn's disease.

BACKGROUND: Recent studies have shown both interleukin 2 (IL-2) and interferon gamma (IFN) to be elevated in patients with active Crohn's disease compared to ulcerative colitis or non-inflammatory bowel disease controls. However the effect of treatment on these lymphokines has not been studied. PATIENTS AND METHODS: Using a reverse haemolytic plaque assay the percentage of lymphokine-secreting cells was determined in the intestinal mucosa of children with Crohn's disease before and after 8 weeks of treatment with either enteral nutrition, cyclosporin or steroids. RESULTS: Before treatment, a high percentage of cells isolated from mucosal biopsies secreted IL-2 or interferon-gamma. Eight weeks' treatment with the immunosuppressive agents cyclosporin, or with corticosteroids, produced a significant reduction in the percentage of IL-2 secreting cells, although only for the former was there also a reduction in interferon-gamma secreting cells. Enteral nutrition however, produced a reduction in lymphokine-secreting cells equivalent to cyclosporin and produced the best histological and clinical improvement. CONCLUSION: Enteral nutrition and cyclosporin can down-regulate lymphokine secretion in the gut in Crohn's disease.

Adolescent↗