Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the influence of immaturity on the responsiveness of enterocytes to specific pathogens, a dose-response curve for cholera toxin (CT)-induced fluid secretion was determined in the proximal small intestine of rats at 2 and 4 wk of age. The suckling rat was approximately 50 times more sensitive to CT in triggering the secretory response than the weaned rat, when estimated by the medium-effective dose (ED50, 0.8 vs. 38.9 nM). Cortisone, known to promote enterocyte maturation, when injected into suckling rats, decreased host sensitivity approximately 1,000 times. Neither age nor cortisone decreased the receptor binding of 125I-labeled CT to intestinal microvillus membranes. In contrast, cortisone treatment caused a threefold increase in receptor density from 14.5 to 43.0 pmol/mg protein. The enzyme responsible for the sodium pump, Na+-K+-ATPase, showed a threefold increase in activity both after weaning and after a cortisone treatment. These data indicate that the immature gut exhibited an increased host sensitivity to CT stimulation that was not correlated with initial receptor binding but was related to a lowered Na+-K+-ATPase activity, suggesting that an underdeveloped sodium pump may be partially responsible for the high incidence of secretory diarrhea in neonates.
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PMID:Age and cortisone alter host responsiveness to cholera toxin in the developing gut. 253 37

Mucin secretion was examined in three functional models relevant to human disease, using rat small intestinal rings or in situ loops, [3H]glucosamine precursor labelling, gel chromatography and a specific radioimmunoassay for mucin. As a model for acute bacterial secretory diarrhoea, tissues were exposed to cholera toxin for up to 4 h. Both stored and newly synthesized radioactive glycoproteins were secreted in amounts twofold to threefold above control levels. Immunoreactive mucin secretion increased fivefold to eightfold. Other agents known to raise cAMP levels did not stimulate mucin secretion, suggesting that cholera may release mucin by a non-cAMP-dependent mechanism. Sepharose 2B chromatography indicated that secreted mucin was smaller in size than intracellular mucin and had compositional differences suggestive of 'immaturity' or protein contamination. In chronically (seven days) reserpinized rats, used as a model of glycoprotein abnormalities relevant to cystic fibrosis, mucin secretion increased twofold to threefold, but the most prominent abnormality was a marked increase in [3H]glucosamine incorporation into all tissue glycoproteins. On purification, the intracellular mucin of reserpine-treated rats had the same composition as mucin from control rats, but the former was smaller in size and had a higher specific radioactivity. Mucin hypersecretion in reserpinized rats may therefore be secondary to a primary and chronic hyperstimulation of mucin biosynthesis. A model of intestinal 'anaphylaxis' or immune-mediated diarrhoea was created in Hooded Lister rats by immunizing with egg albumin (10 micrograms) and challenging with the same antigen in intestinal loops 14 days later. After 4 h, total protein, DNA and brush border sucrase were increased in the lumen. Enhancement of mucin secretion did not occur, however, and therefore does not seem to be a particular feature of the pathophysiology of this model.
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PMID:Acute and chronic models for hypersecretion of intestinal mucin. 656 39

Malnourished rats during suckling were orally immunized with cholera toxin (CT) after different periods of refeeding. Intestinal fluids, sera, and supernatant fluids from cultured mesenteric lymph node (MLN) cells were obtained after rats were given three doses of CT and analyzed by enzyme-linked immunosorbent assay (ELISA) to evaluate the specific antibody response. Serum-specific immunoglobulin G (IgG), IgA, and IgM were severely diminished in malnourished rats immunized with three doses of CT after 1 week of refeeding when compared with those of controls. Also, a decreased IgA ELISA titer of the intestinal fluids and abrogation of the capacity to neutralize the CT in the intestinal ligated loop test were found. When a booster was given at 113 days of age, the immune response continued to be affected in the serum and the intestinal fluid. The results from the analysis of the supernatant fluids from cultured MLN cells were coincident with those mentioned above. When one dose of CT was administered into Peyer's patches (PP) after 1 week of refeeding, an impaired immune response was found in the intestinal fluid of malnourished rats during suckling compared with that of controls. This result together with the analysis of supernatant from MLN and PP cell cultures suggests that antigen triggering in the PP was affected. When the refeeding period was extended to 30 days and then the first dose of CT was administered, the antibody immune responses in intestinal fluid serum and supernatant fluid approached control values. These observations reinforce the fact that the gut-associated lymphoid tissue immaturity of the rats when they received the first CT dose (at 28 days old) was the main reason for the decreased immune response observed in the experimental group.
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PMID:Deficient induction of the immune response to oral immunization with cholera toxin in malnourished rats during suckling. 792 75