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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The technique of rapid (60 seconds) acid treatment of intact rat bladders was used to evaluate bacterial interactions with bladder mucin and mucosal cells. Using the rat model system, SEM indicated that short term acid treatment removed the mucin layer but it also modified the bladder epithelial cell surface. Although the treatment which removed mucin allowed an increase in random bacterial attachment, the increase could also be attributable to acid modification of the mucosa. Examination of acid treated rabbit bladders also showed mucin removal and simultaneously bladder epithelium modification. We conclude that short term acid treatment removes mucin, modifies the epithelial layer, and appears to nonspecifically increase bacterial attachment on the mucosa by modifying the mucosal surface.
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PMID:Evaluation of bacterial attachment to acid treated bladder epithelium. 676 51

A possible thermodynamic mechanism for the inhibition of bacterial adhesion to the epithelial bladder surface was investigated in rabbits. Contact angles of aqueous polymeric droplets were measured to assess the relative hydration and surface-free energy, of normal and mucin-free bladder surfaces. We measured an angle of 91.2 +/- 1.2 degrees (SEM), n = 37 for the intact mucin surface and an angle of 120.5 +/- 1.2 degrees, n equal 46 for the epithelium after the mucin was removed with acid. These results indicate that mucin makes the epithelial surface significantly more hydrophilic and so produces a very low free energy interface with the urine environment. Such a low energy surface would inhibit bacterial adhesion because the surface already exists at its free energy minimum.
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PMID:Rabbit bladder-surface mucin: a thermodynamic mechanism for inhibiting bacterial adhesion. 686 23

Escherichia coli RDEC-1 (serotype O15:H-) is a rabbit enteropathogen in which in vivo enteroadherence is both site specific and age related. To determine whether these differences could be related to mucins, we evaluated inhibition of binding of AF/R1 piliated RDEC-1 by mucins isolated from various segments of intestine of rabbits at different ages. Mucin was purified from intestinal crude mucus by cesium chloride serial ultracentrifugation. RDEC-1 was grown to promote the expression of hydrophobic mannose-resistant AF/R1 pili. Quantitation of in vitro bacterial binding was determined using a crystal violet colorimetric assay. In postweanling rabbits, inhibition of RDEC-1 binding by purified mucin derived from ileal segments (45.1 +/- 2.6%, mean +/- SEM) and proximal colonic segments (46.0 +/- 5.5%) was less than purified mucins derived from jejunal segments (70.0 +/- 2.0%) and distal colonic segments (71.0 +/- 3.7%, p < 0.05) of the intestinal tract. In all age groups, mucins derived from jejunal segments inhibited RDEC-1 binding to a greater level than mucins derived from ileal segments. In addition, inhibition of binding by mucin derived from proximal small intestine of postweanling rabbits (70.0 +/- 2.0%) was greater than that of weanling rabbits (55.2 +/- 3.5%, p < 0.05) with suckling rabbit inhibition (62.1 +/- 3.5%) between these two levels. We conclude that mucin inhibition of RDEC-1 adhesion is both age and region related and therefore may contribute to both age-related and site localization of bacterial infections of the intestinal tract.
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PMID:Disparate in vitro inhibition of adhesion of enteropathogenic Escherichia coli RDEC-1 by mucins isolated from various regions of the intestinal tract. 770 Jul 37

To determine whether induced sputum samples might provide a useful means for evaluating the effects of therapy on airway mucosal inflammation, we examined induced sputum samples obtained before and after 6 days of treatment with prednisone (0.5 mg/kg/day) or placebo in a randomized, double-blind study of 24 asthmatic subjects. Induced sputum was analyzed for total and differential cell counts and for concentrations of eosinophil cationic protein, albumin, and mucin-like glycoprotein. We found that the mean (+/- SEM) percentage of eosinophils in sputum samples from the prednisone-treated group fell from 14.1% +/- 5.0% at baseline to 1.8% +/- 0.8% after treatment, a decrease significantly greater than in the placebo-treated group (from 10.3% +/- 4.9% to 11.1% +/- 4.0%; p = 0.002). The absolute number of eosinophils also decreased significantly more in the prednisone-treated group than in the placebo-treated group (p = 0.04). In addition, eosinophil cationic protein levels in induced sputum fell more in the prednisone-treated group than in the placebo-treated group (from 324 +/- 131 ng/ml to 144 +/- 84 ng/ml vs 173 +/- 50 ng/ml to 188 +/- 47 ng/ml; p = 0.002). Furthermore, prednisone treatment was associated with a significant increase in peak expiratory flow, an effect that was significantly correlated with the decrease in eosinophil percentage in induced sputum (rs = 0.64, p = 0.04). Prednisone treatment was not associated with any significant change in the concentrations of albumin or mucin-like glycoprotein. We conclude that analysis of induced sputum is a useful noninvasive method for studying the effects of asthma therapy on airway eosinophilic inflammation.
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PMID:Analysis of induced sputum to examine the effects of prednisone on airway inflammation in asthmatic subjects. 796 55

Previous studies using the CA 19-9 antibody have demonstrated that serum mucin levels in patients with cystic fibrosis (CF) are elevated and that the degree of elevation relates to the age of the patient and possibly to his or her clinical status. However, CA 19-9 only recognizes the mucin-associated blood group sialyl Le(a+) antigen, so mucin levels cannot be measured in patients without Lewis antigens. The present study used the 17B1 monoclonal antibody to measure serum mucin levels in normal subjects, and in patients with CF, patients with chronic obstructive pulmonary disease (COPD), and patients with lung transplants. Serum mucin levels were 25 ng/ml (+/- 1 SEM, n = 8) in normal subjects, 13,853 ng/ml (+/- 1,281, n = 25) in patients with CF, and 25.5 ng/ml (+/- 1.9, n = 17) in patients with COPD. Patients with CF who were sialyl Le(a-b-) also had elevated serum mucin levels (715 +/- 152, n = 2). Serum mucin levels of six lung transplant recipients with CF were elevated compared with those in normal subjects (4,621 +/- 765 ng/ml), but they were not different from serum mucin levels in six lung transplant recipients without CF (5,307 +/- 1.677 ng/ml). Preliminary characterization of the serum mucin antigen showed that: (1) in CF sera, the antigen is polydisperse and smaller than the antigen in normal sera; (2) the mucin antigen is distinct from ABO blood group antigens. Serum mucin levels may be a useful marker to follow a specific patient's response to therapy.
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PMID:Elevated levels of serum mucin-associated antigen in adult patients with cystic fibrosis. 834 2

To determine whether markers of mucus secretion can be quantified in airway lining fluid from asthmatic and from healthy subjects, we measured levels of a mucin-like glycoprotein (MLG) and lactoferrin in sputum induced by inhalation of hypertonic (3%) saline in 18 asthmatic and in 10 healthy subjects. Because DNA, like mucin, contributes to the viscosity of airway secretions, we also measured DNA levels in the induced sputum samples. To control for the presence of saliva in sputum, we also analyzed saliva samples from all subjects. The entire sputum sample and the saliva sample were reduced using dithiotreitol, and biochemical analysis was performed on supernatants obtained after centrifugation. We found that induced sputum from asthmatic subjects had higher levels of MLG [2,574.4 +/- 907.8 (mean +/- SEM) versus 562.2 +/- 90.5 micrograms/ml, p < 0.007] and DNA (7.1 +/- 1.6 versus 3.6 +/- 0.6 micrograms/ml, p < 0.05), but the difference in lactoferrin levels failed to reach statistical significance. However, in the subgroup of asthmatic subjects who gave a history of sputum production (n = 9), lactoferrin levels were higher than in the healthy control subjects (118.9 +/- 46.3 versus 35.2 +/- 6.5 micrograms/ml, p < 0.05). The very low levels of MLG, DNA, and lactoferrin measured in saliva were not significantly different in asthmatic subjects from those in healthy subjects. We conclude that measurement of markers of mucus secretion in induced sputum is feasible in asthmatic and healthy subjects, and it reveals abnormally high markers of mucus secretion in subjects with stable asthma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Markers of mucus secretion and DNA levels in induced sputum from asthmatic and from healthy subjects. 848 21

The exact mode of action of topical nasal corticosteroids is still uncertain. The aim of this study was to determine their effects on microvascular permeability and cellular and glandular secretion by measuring the levels of total protein, albumin, lysozyme and mucin recovered in nasal lavage fluid before and after 3 weeks of treatment with a topical nasal corticosteroid in 12 normal non-atopic subjects. Six subjects applied 200 micrograms fluticasone propionate and six applied 200 micrograms beclomethasone dipropionate to one nostril in each 24 h: matched placebo was applied to the other nostril. There was a significant rise in the level of mucin recovered compared with baseline values following fluticasone administration (baseline 76.2 micrograms/ml (mean) +/- 5.5 (SEM), fluticasone 118.3 micrograms/ml +/- 11.6 P = 0.015) and beclomethasone administration (baseline 64.3 micrograms/ml +/- 6.6, beclomethasone 87.2 micrograms/ml +/- 4.8, P = 0.041). There was no significant change in the levels of total protein, albumin or lysozyme following either active medication or placebo treatment. Topical corticosteroids appear to potentiate mucin secretion and do not alter serous secretion or microvascular permeability in the unchallenged non-atopic nose.
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PMID:Topical corticosteroids potentiate mucin secretion in the normal nose. 867 28

Damage to the gastrointestinal tract mucous layer may render underlying cells susceptible to intraluminal toxins or carcinogens. Our aim was to determine the effect of bile acids on mucin, the primary constituent of mucous. Differentiated Caco-2 and HT29 cells were used as models of human colonic epithelial cells. Mucin was measured by [3H]-glucosamine labeling. Short term (30 min) incubations with 1-5 mM unconjugated bile acids or taurodeoxycholic acid induced mucin release relative to bile acid hydrophobicity. Longer incubations were cytotoxic. Long term (7 days) incubation at nontoxic concentrations (0.1 mM) of deoxycholic acid (DC) decreased total mucin by 36 +/- 2% (SEM, P = 0.0003) in differentiated HT29 cells and by 57.2 +/- 2% (P < 0.05) in Caco-2 cells. Tauroursodeoxycholic acid (TUDC) or ursodeoxycholic acid (0.1-0.5 mM) did not alter mucin levels. Simultaneous incubation of 0.1 mM DC and 0.1-0.5 mM TUDC or 2.5 mM TDC and TUDC did not change mucin levels. Differentiated HT29 and Caco-2 cells contained high levels of intestinal mucin MUC3 mRNA while undifferentiated HT29 cells did not possess a MUC3 message. Deoxycholic acid (0.1 mM) did not alter the MUC3 mRNA level. Neither cell type showed detectable expression of intestinal MUC2 or gastric MUC6. Thus, cytotoxic concentrations of bile acids induce mucin release, presumably due to detergent effects. Nontoxic concentrations of DC reduce mucin levels in differentiated enterocyte-like cells, which can be prevented by coincubation with TUDC. The bile acid-induced alterations in mucin production by enterocytes observed in vitro may influence intestinal cytoprotection in vivo.
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PMID:Bile acid-induced alterations of mucin production in differentiated human colon cancer cell lines. 872 6

Increased serum levels of mucin-associated antigen have been previously demonstrated in patients with cystic fibrosis (CF) and interstitial pneumonia, and in lung-transplant recipients. The present study assessed the serum airway mucin levels in patients with acute respiratory distress syndrome (ARDS). An enzyme-linked immunosorbent assay (ELISA) method with a human-airway-mucin-specific monoclonal antibody (17Q2) was used to measure serum mucin levels in normal subjects, chronic smokers, patients with chronic bronchitis and other pulmonary diseases, patients with acute cardiogenic lung edema, and patients with ARDS. The serum mucin levels measured 9.9 +/- 0.8 ng/ml (mean +/- SEM, n = 59) in normal subjects, 12.7 +/- 1.6 ng/ml (n = 29) in chronic smokers, 21.8 +/- 1.9 ng/ml (n = 28) in patients with chronic bronchitis and other pulmonary diseases, 9.0 +/- 3.1 ng/ml (n = 5) in patients with acute cardiogenic lung edema. The serum mucin level was 53.8 +/- 6.6 ng/ml (n = 13) in patients with ARDS (p < 0.05, as compared with the four other groups). Serial measurements of serum mucin levels were obtained in patients with ARDS. Statistical analysis showed an inverse correlation of serial measurements of serum mucin with static respiratory-system compliance (p = 0.021), an inverse correlation of sequential serum mucin levels and log(Pa(O2)/Fl(O2)) (p = 0.016), and a positive correlation of sequential serum mucin levels and lung injury score (LIS) (p = 0.019). Gel-filtration analysis showed that mucin-associated antigens in ARDS sera were polydispersed and smaller than the antigens in normal sera. This study indicates that an increasing amount of degraded mucin occurs in patients with ARDS.
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PMID:Elevated serum levels of mucin-associated antigen in patients with acute respiratory distress syndrome. 937 60

1. Polyriboinosinic-polyribocytidylic acid (Poly I:Poly C), an interferon inducer was studied for its effect on gastric ulceration in rats. Polyriboinosinic-polyribocytidylic acid (1, 2 and 4 mg/kg, i.m.) showed a dose-dependent inhibition of gastric ulcers induced by aspirin, cold restraint stress and pylorus ligation (Shay's model). Protective dose (PD50) +/- SEM values of Poly I:Poly C on these models of ulcers were 1.9 +/- 0.2, 2.3 +/- 0.4 and 2.8 +/- 0.4 (mg/kg, i.m.) respectively. 2. Polyriboinosinic-polyribocytidylic acid (10-60 micrograms) produced dose-dependent inhibition of gastric proton pump (H+/K(+)-ATPase) activity in the gastric parietal microsomal fraction. The concentration of Poly I:Poly C causing a 50% inhibition (IC50) +/- SEM was found to be 17.6 +/- 1.2 micrograms. 3. Polyriboinosinic-polyribocytidylic acid caused a significant decrease in free and total acid and pepsin and an increase in mucin content in Shay (pylorus-ligated) rat. 4. Polyriboinosinic-polyribocytidylic acid did not exert a significant influence on isolated tissue preparations for anti-cholinergic (acetylcholine-induced contraction of guinea-pig ileum) and H2-anti-histaminic (histamine-induced contraction of rat uterus and guinea-pig auricle) activities. 5. Thus, the present study indicates that Poly I:Poly C may possess anti-gastric ulcer activity as a result of inhibition of the gastric proton pump.
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PMID:Interferon-inducer polyriboinosinic-polyribocytidylic acid: a potent anti-gastric ulcer agent and inhibitor of the gastric proton pump in rats. 967 29


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