Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NASAL MUCOSA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

A study of the synthesis and inactivation of prostaglandin E by pig nasal mucosa.

Prostaglandins of the E series have been shown to be more potent than adrenaline as nasal decongestants. We now present evidence that prostaglandins of the E series (PGE) can be synthesised and inactivated by the nasal mucosa of the pig. This study demonstrates that PGE may be formed by pieces of pig nasal mucosa in vitro and that PGE formation by the nasal mucosa is inhibited by indomethacin. The nasal mucosa was also shown to contain 15-hydroxy prostaglandin dehydrogenase activity and this enzyme is involved in the inactivation of PGE. The findings of this study may help towards a better understanding of the role of PGE in nasal physiology and nasal disease.

Animals↗
PubMed1994

Study on the IL-5 expression in allergic nasal mucosa.

An immunohistological study was performed on allergic and nonallergic nasal mucosa to examine interleukin-5 (IL-5) expression. Many cells in the superficial portion of lamina propria expressed IL-5 in allergic nasal mucosa, whereas few cells expressed IL-5 in nonallergic mucosa. Furthermore, it was suggested by immunohistological double staining that CD45RO-positive cells, EG2-positive cells and metachromasia-positive cells expressed IL-5 in allergic nasal mucosa.

Antibodies, Monoclonal↗
PubMed1997

DNA adducts in human nasal mucosa and white blood cells from smokers and non-smokers.

The goal of the present study was to measure the levels of DNA adducts in human nasal mucosa cells and in total white blood cells in relation to smoking. DNA was isolated from samples of 20 healthy volunteers (six smokers and 14 non-smokers). The levels of DNA adducts were measured by 32P-postlabelling assay. In smokers the mean DNA adduct levels were 3.3 and 17.0 adducts/10(8) nucleotides in total white blood cells and nasal mucosa cells respectively. The corresponding values in non-smokers were 2.0 and 6.8 adducts/10(8) nucleotides. The mean adduct level was significantly higher in nasal mucosa cells than in total white blood cells both in smokers and non-smokers. The mean adduct levels in smokers' nasal mucosa cells were significantly higher than those in non-smokers. Thus the nasal mucosa cells constituted a sensitive tissue for the determination of cigarette smoking induced DNA adducts. Combining the sensitivity of the 32P-postlabelling assay with the specificity of the nasal mucosa to the airborne chemical exposures, the DNA adduct analysis from human nasal mucosa cells represents a method of choice in the assessment of exposure to airborne carcinogens.

Adult↗
PubMed1984

Mechanisms for reflexive hypertension induced by local application of capsaicin and nicotine to the nasal mucosa.

The cardiovascular effects of locally applied nicotine and capsaicin to the nasal mucosa were studied in anaesthetized guinea-pigs. Local application of capsaicin (0.3-30 microM) or nicotine (0.3-30 mM) induced dose-dependent increases in arterial blood pressure, mainly due to an increase in peripheral vascular resistance. The capsaicin and nicotine responses were abolished after local anaesthesia and markedly reduced (to about 20% of control) by combined pretreatment with phentolamine and propranolol, suggesting reflexogenic sympathetic activation. Systemic capsaicin pretreatment abolished the hypertensive effect of capsaicin (30 microM) and reduced the response to nicotine application to about 25% of control (p less than 0.001). Local capsaicin pretreatment of the nasal mucosa one week earlier also significantly reduced the capsaicin response (p less than 0.05), while the nicotine-induced increase in blood pressure was not significantly changed. The present findings suggest the presence of two afferent mechanisms in the nasal mucosa which induce hypertension upon chemical irritation. The capsaicin response is dependent upon capsaicin-sensitive afferents. The nicotine response involves mainly capsaicin-sensitive neurons and, in addition, a minor component which is resistant to capsaicin pretreatment. Thus, the hypertensive effect of nicotine applied locally to the nasal mucosa seems to be mainly mediated via sensory mechanisms other than the sneezing response which is not dependent on capsaicin sensitive nerves.

Administration, Intranasal↗
PubMed2005

[Expression of eotaxin gene in nasal mucosa of allergic rhinitis in the guinea pig sensitized by fungal allergen].

OBJECTIVE: To study the expression and significance of Eotaxin gene in nasal mucosa of guinea pig sensitized by fungal allergen. METHOD: Alternaria alternata sensitized guinea pigs used as animal model of allergic rhinitis (AR). The changes in the nasal mucosa were studied by pathological method and the Eotaxin gene were studied by In Situ Hybridization. RESULT: The behavior science score of experimental group was significant higher than the controls group. Plenty eosinophils were found in lamina propria of nasal mucosa of experimental group. Eotaxin gene is expressed in lamina propria of nasal mucosa of experimental group. The controls group had not positive expression. CONCLUSION: Eotaxin gene is expressed at high levels in nasal mucosa of fungal allergic rhinitis in the guinea pig. Plenty eosinophils were found in nasal mucosa. We considered that Eotaxin gene and eosinophils could play a key role in fungal allergic rhinitis.

Alternaria↗
PubMed2006

[Differential proteins analysis for human nasal polyposis and normal nasal mucosa].

OBJECTIVE: To establish two-dimensional polyacrylamide gel electrophoresis (2-DE) map with high resolution and reproducibility from human nasal polyposis and normal nasal mucosa, and to identify differential expression proteins of 2-DE map. METHOD: Samples of human nasal polyposis and normal nasal mucosa (each sample group containing seven cases) were obtained. The total proteins were extracted and separated by immobilized pH gradient (IPG)-based 2-DE. The silver-stained 2-DE were scanned with digital Image Scanner and analyzed with ImageMaster 2-DE Elite 4.01 software. Peptide mass fingerprint (PMF) of differential protein spots was obtained with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). The peptide mass fingerprints were searched in Swiss-Prot and TreMBL database by PeptIdent software, and then differential expression proteins were identified. RESULT: (1) 2-DE for a randomly selected 1 sample from each of the 2 groups was repeated 3 times respectively to analyze the reproductive of the method. The image analysis showed: For the polyposis tissues, the average proteins spots of three 2-DE maps were 891 +/- 67 and 767 +/- 83, spots were matched with the average matching rate of 86.1%. The average deviations of matched spot position were (1.13 +/- 0.16) mm in IEF direction and 1.45 +/- 0.21) mm in SDS-PAGE direction, respectively. For the nasal mucosa tissues, the average proteins spots of three 2-DE maps were 936 +/- 62 and 821 +/- 78, spots were matched with the average matching rate of 87.7%. Comparing the average electrophoresis profiles of the two tissues, each sample contained 7 cases. The proteins spots of nasal polyposis and nasal mucosa tissues were 1532 and 1617. A total of 1 065 proteins spots were matched between the two tissues average electrophoresis profiles. (2)Twenty dif-ferential expression protein spots were incised from silver staining gel randomly and digested in gel by TPCK Trypsin. Sixteen PMF were obtained by MALDI-TOF-MS, and 11 differential expression proteins were identified. CONCLUSION: In this study, the well-resolved reproducible 2-DE map of human nasal polyposis and nasal mucosa were established. Certain differential proteins were identified.

Adult↗
PubMed2004

Expression of annexin A1 in normal and chronically inflamed nasal mucosa.

OBJECTIVE: To examine the expression pattern of annexin A1 in normal and chronically inflamed nasal mucosa to investigate its possible role in nasal inflammation. DESIGN: Immunohistochemical analysis. SUBJECTS: Samples of middle turbinates from 5 healthy subjects and 5 patients with perennial rhinitis, and samples of nasal polyps from 7 patients. INTERVENTIONS: Annexin A1 expression was examined with a standard immunohistochemical protocol on paraffin-embedded sections. RESULTS: Annexin A1 was highly expressed by ciliated cells, where it was concentrated on the apical surface and within the cilia. Goblet cells and nondifferentiated basal epithelial cells did not stain. In the glands of the lamina propria, intense staining was found in the cytoplasm and in the nuclei of the cells in the duct epithelium, whereas acinar cells did not stain. Intense cytoplasmic staining was observed in infiltrating polymorphonuclear cells and macrophages. No differences in the pattern or the level of expression of annexin A1 were found in the epithelial cells and glands of normal and chronically inflamed (perennial rhinitis or polyps) nasal mucosa. CONCLUSION: These results suggest that the expression of annexin A1 in respiratory epithelium of nasal mucosa is related to cell type and differentiation status of the cells and is not significantly altered by inflammatory diseases.

Annexin A1↗
PubMed1987

Metachromatic cell progenitors and specific growth and differentiation factors in human nasal mucosa and polyps.

We previously demonstrated that fluctuations in circulating metachromatic cell progenitors were inversely related to nasal metachromatic cell (NMC) counts and nasal symptoms in allergic rhinitis. Now, we have quantitated NMC progenitors and lineage-specific growth factors using a hemopoietic colony assay. Cell suspensions from excised collagenase-treated nasal polyps (n = 7) contained 3.8 +/- 1.1 granulocyte colony-forming cells per 10(6) cells plated, compared to less than or equal to 0.5 in human tonsil suspensions, less than or equal to 0.5 in nasal mucosal epithelial scrapings, and 33 +/- 8 in peripheral blood of patients with ragweed allergic rhinitis (p less than 0.01). The percentage of metachromatic cells in nasal-polyp-derived colonies was 47 +/- 10 compared with 3.0 +/- 0.7 in peripheral blood colonies (p less than 0.005). Highly potent metachromatic cell colony-stimulating activity (CSA) was detected in supernatants from cultured human nasal epithelial scrapings from both polyps and atopic nasal mucosa, but not from nonatopic nasal mucosa. Supernatants from polyp mononuclear cells stimulated with phytohemagglutinin also contained metachromatic cell-CSA, which had an approximate molecular size of 25 to 70,000 daltons on column chromatography. An IL-3-like activity was also detected in these supernatants. These observations provide further evidence for in situ hemopoietic mechanisms in human nasal mucosa, involving epithelium-derived stimulation of local metachromatic cell progenitor growth and differentiation in allergic rhinitis.

Basophils↗
PubMed1997

Detection of DNA adducts in human nasal mucosa tissue by 32P-postlabeling analysis.

Nasal epithelium is an easily accessible tissue that is potentially useful for human biomonitoring studies aimed at evaluating exposure to airborne carcinogens. We have devised a simple technique, which causes minimum distress to the informed patient, to obtain very small but sufficient biopsies from the inferior or middle turbinate head. DNA adducts were measured by 32P-postlabeling assay in nasal mucosa of nine cigarette smokers (including two subjects who had given up smoking shortly before sampling), two former smokers and 10 non-smoker healthy donors. None of the subjects reported other recent exposures to mutagens or carcinogens. Using the nuclease P1 technique, a mean adduct level of 4.8/10(8) bases and a specific spot pattern, the diagonal radioactive zone, were found in smokers, whereas non-smokers showed a significantly lower global level of DNA adducts, i.e. 1.4/10(8) bases, and no diagonal zone. Another important result was the presence of a significant association between DNA adduct level and the number of cigarettes smoked daily. These preliminary findings suggest that the level of DNA adducts measured from biopsies of the nasal mucosa is a reliable marker of exposure to cigarette smoking and uphold its use in biomonitoring exposures to other airborne DNA binding compounds.

Adolescent↗
PubMed2004

Effects of dioxane on cytochrome P450 enzymes in liver, kidney, lung and nasal mucosa of rat.

The effect of acute and chronic dioxane administration on hepatic, renal, pulmonary and nasal mucosa P450 enzymes and liver toxicity were investigated in male rats. The acute treatment consisted of two doses (2 g/kg) of dioxane given for 2 days by gavage, whereas the chronic treatment consisted of 1.5% of dioxane in drinking water for 10 days. Both the acute and chronic dioxane treatments induced cytochrome P450 2B1/2- and P450 2E1-dependent microsomal monooxygenase activities (pentoxyresorufin O-depentylase and p-nitrophenol hydroxylase) in the liver, whereas in the kidney and nasal mucosa, only the 2E1 marker activities were enhanced. In addition in the liver, an induction of 2alpha-testosterone hydroxylase (associated with the constitutive and hormone-dependent P450 2C11) was also revealed, whereas the hepatic P450 4A-dependent omega-lauric acid hydroxylase was not enhanced by any dioxane treatment. These inductions were mostly confirmed by western blot analysis of liver, kidney and nasal mucosa microsomes. In the lung, no alteration of P450 activities was observed. To assess the mechanism of 2E1 induction, the hepatic, renal and nasal mucosa 2E1 mRNA levels were also examined. Following two kinds of dioxane administration, in the liver the 2E1 induction was not accompanied by a significant alteration of 2E1 mRNA levels, while both in the kidney and nasal mucosa the 2E1 mRNA increased about 2- to 3-fold, indicating an organ-specific regulation of this P450 isoform. Furthermore, dioxane was unable to alter the plasma alanine aminotransferase activity and hepatic glutathione (GSH) content, examined as an index of toxicity, when it was administered into rats with P450 2B1/2 and 2E1 preinduced by phenobarbital or fasting pretreatment. These results support the lack of or a poor formation of reactive and toxic intermediates during the biotrasformation of this solvent, even when its metabolism was enhanced by P450 inducers. The chronic administration of dioxane was also unable to induce the palmitoyl CoA oxidase, a marker of peroxisome proliferation, excluding this as a way to explain its toxicity. Thus, although the mechanism of dioxane carcinogenicity remains unclear, the present results suggest that the induction of 2E1 following a prolonged administration of dioxane might provide oxygen radical species, and thereby contribute to its organ-specific toxicity.

Administration, Oral↗
PubMed2006

Gene and protein expression of protease-activated receptor 2 in structural and inflammatory cells in the nasal mucosa in seasonal allergic rhinitis.

BACKGROUND: Protease-activated receptor 2 (PAR 2) has been shown to be responsible for trypsin and mast cell tryptase-induced airway inflammation. Here, the present study aimed to explore the expression of PAR 2 in the nasal mucosa of seasonal allergic rhinitis (SAR). METHODS: Study subjects were recruited for the study by medical history, physical examination and laboratory screening tests. Using immunohistochemistry, laser-assisted cell picking and subsequently real-time PCR, nasal mucosa biopsies of SAR patients were investigated for PAR 2 gene and protein expression in complex tissues of the nasal mucosa. RESULTS: Gene and protein expression of PAR 2 was firstly detected in nasal mucosa of SAR patients. The relative gene expression level of PAR 2 was significantly increased in complex tissues of the nasal mucosa of SAR (6.21+/-4.02 vs. controls: 1.38+/-0.86, P=0.004). Moreover, PAR 2 mRNA expression in epithelial cells (SAR: 4.78+/-4.64 vs. controls: 0.84+/-0.61, P=0.003) but not in mucus (SAR: 1.51+/-1.15 vs. controls: 1.35+/-1.02, P=0.78) and endothelial cells (SAR: 1.20+/-0.57 vs. controls: 1.73+/-1.30, P=0.5) was found to be significantly changed in the nasal mucosa in SAR. Using double immunohistochemistry the present study demonstrated that the total numbers of mast cells (P=0.0003) and eosinophils (P=0.03) and the numbers of eosinophils expressing PAR 2 (P=0.006) were significantly elevated in the nasal mucosa of SAR compared with the controls. CONCLUSION: The abundant presence and distribution of gene and protein expression of PAR 2 in different cell types in the nasal mucosa under normal situation, the increased expression of PAR 2 in epithelial cells and the increased number of eosinophils with PAR 2 suggest that PAR 2 may contribute to the pathogenesis of allergic diseases such as SAR.

Adolescent↗
PubMed2004

[Influence of seven absorption enhancers on nasal mucosa--assessment of toxicity].

OBJECTIVE: To study the influence of seven different absorption enhancers on nasal mucosa. METHODS: By testing last time of ciliary movement, velocity of ciliary movement, ciliary structural and specific cellular changes of nasal mucosa the influence of seven different absorption enhancers on nasal mucosa. RESULTS: The effect on lasting time of ciliary movement was 1%SDS>1%SDC>1%Brij35>5%Tween80>0.1%EDTA>5%HP-beta-CD>1%lecithin the effect on velocity of ciliary movement 1%Brij35>1%SDC>1%SDS>0.1%EDTA>1%lecithin>5%Tween80>5%HP-beta-CD,and the effect on ciliary structural and specific cellular changes of nasal mucosa 1%SDS approximately 1%SDC approximately 1%Brij35>5%Tween80>0.1%EDTA approximately 5% HP-beta-CD approximately 1%lecithin. CONCLUSION: The three methods have good correlation.

Absorption↗
PubMed2005

[Cytological evaluation of the nasal mucosa in healthy children born before 37 weeks of gestation].

Cytological evaluation of the nasal mucosa is one of the methods used in the diagnosis of upper respiratory diseases. Cytological examination of the nasal mucosa in very young children have sporadically been performed. In our study the evaluation was performed in Neonatal Units. Cytograms of 80 new-born children of both sexes were evaluated. All the infants were born prematurely. Cytograms of the nasal mucosa of new-born children differ from these of adults and older children. Either columnar cells or neutrophils are prevalent in cytograms of the healthy new-born children. Goblet cells do not occur. Cytological evaluation of nasal mucosa as non-invasive and easy to perform examination can be very useful in screening of the very young children with a risk of respiratory system disorders.

Cytodiagnosis↗
PubMed2002

The effects of water-soluble cyclodextrins on the histological integrity of the rat nasal mucosa.

The aim of this study was to investigate the effect of highly water-soluble cyclodextrins (CDs) on the histological integrity of the nasal mucosa. In order to evaluate their effects, the in vivo single and repeated nasal exposure studies were performed using male Wistar rats. The rat nasal cavity was excised after an application of various CD solutions at different times. The morphological appearances of the rat nasal mucosae were analyzed with the light microscopic and the scanning electron microscopic studies. By utilizing 5-min exposure of each CD solution to the nasal mucosa, no tissue damage was visible for 1.5% w/v beta-CD and 5 and 20% w/v hydroxypropyl beta-CD (HP beta-CD), and the effects were quite similar to controls. However, using 20% w/v randomly methylated beta-CD (RM beta-CD) showed severe damage on the integrity of nasal mucosa. The severity was similar to 1% w/v polyoxyethylene-9-lauryl ether or l% w/v sodium deoxycholate. Meanwhile, 30 or 60 min exposure to 10% w/v HP beta-CD or RM beta-CD resulted in no obvious mucosal damage. In addition, in vivo repeated dosing of RM beta-CD did not show any toxicity up to 20% w/v. These results suggest that at least, less than 10% w/v CD solutions do not induce gross tissue damage and can keep the histological integrity of the nasal mucosa.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed2001

Fluticasone propionate aqueous nasal spray reduces inflammatory cells in unchallenged allergic nasal mucosa: effects of single allergen challenge.

BACKGROUND: Topical corticosteroid therapy reduces symptoms and nasal mucosal inflammatory cells in patients with allergic rhinitis. Usually patients are advised to start their medication (1 week) before the beginning of the pollen season. The effect of pretreatment with a topical corticosteroid on unchallenged nasal mucosa is not well documented. OBJECTIVES: The purpose of this study was to investigate, in a double-blind, placebo-controlled study, the effect of 6 weeks' pretreatment with 200 microg twice daily fluticasone propionate on nasal symptoms and inflammatory cell numbers after nasal allergen provocation in patients with seasonal allergic rhinitis. METHODS: Nineteen patients with grass pollen-induced allergic rhinitis were treated for a 6-week period out of the grass pollen season. After completing the treatment period, patients were challenged with grass pollen. Nasal mucosal biopsy specimens were taken 5 times in every patient. In nasal mucosa changes in numbers of T cells, B cells, mast cells, eosinophils, macrophages, and Langerhans' cells were investigated. RESULTS: After 4 weeks of treatment but before allergen provocation, significantly fewer epithelial Langerhans' cells, macrophages, mast cells, T cells, and eosinophils were found in the fluticasone propionate group compared with those found in the placebo group. In the lamina propria significantly fewer Langerhans' cells and eosinophils were found in the fluticasone propionate group. Cell influx in nasal mucosa after allergen provocation was significantly inhibited in the fluticasone propionate group compared with that in the placebo group for epithelial Langerhans' cells, mast cells, macrophages, and T cells and for lamina propria eosinophils, mast cells, Langerhans' cells, macrophages, and T cells. CONCLUSIONS: Fluticasone propionate is effective in reducing early- and late-phase nasal symptoms. Topical corticosteroid treatment reduces inflammatory cells in unchallenged nasal mucosa.

Administration, Intranasal↗
PubMed2000

Effect of brief exposure to mitomycin C on cultured human nasal mucosa fibroblasts.

PURPOSE: To observe the effect of mitomycin C (MMC) on cultured human nasal mucosa fibroblasts. METHODS: Cultured human nasal mucosa fibroblasts were exposed to MMC (0.1-0.4 mg/ml) for 1 to 5 minutes. The viability of the fibroblasts was determined by MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay; DNA fragmentation (apoptosis) by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL); apoptotic percentage by flow cytometry; and morphology by light microscopy. RESULTS: A portion of the fibroblasts survived the mitomycin treatment and showed evidence of regrowth within 2 to 3 days. These cells reached confluence in 5 to 7 days. The inhibition rates by MTT assay of 0.4 mg/ml MMC for 5-minute exposures was 31.3%. Dose-response effect was noted with the lower concentrations and shorter exposure times where the inhibition rates were lower (but not significantly so). DNA fragmentation was observed in fibroblasts 24 hours after MMC exposure (0.4 mg/ml) for 5 minutes compared with normal control. The apoptotic rate of fibroblasts treated by 0.4 mg/ml MMC was significantly higher than the control (p < 0.05). CONCLUSIONS: Short MMC exposure times have a variable cytotoxic effect and inhibit proliferation of cultured nasal mucosa fibroblasts. MMC also can induce apoptosis with a 5-minute exposure time. Therefore, it is possible that MMC has a complex effect in dacryocystorhinostomy.

Alkylating Agents↗
PubMed1982

Neurophysiological mechanism of shrinkage of nasal mucosa induced by exercise.

Change of serum norepinephrine level and nasal patency were measured in 10 normal volunteers during exercise and effect of unilateral cervical sympathetic ganglion block on exercise-induced shrinkage of nasal mucosa was evaluated. Serum norepinephrine elevated markedly after 10-min exercise. Unilateral blocking of cervical ganglion completely inhibited mucosal shrinkage induced by exercise in 8 of 10 subjects. Mucosal shrinkage during exercise in these subjects was assumed to be mediated through cervical sympathetic ganglion, and not by increase in circulating cathecolamine. However, in 2 subjects, moderate shrinkage of the nasal mucosa was observed in 10-min after initiation of exercise. It was impossible to rule out some effect of circulating cathecolamine on the capacitance vessels of the nasal mucosa completely.

Adolescent↗