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César Picado - One of the best experts on this subject based on the ideXlab platform.
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dynamics of cox 2 in Nasal Mucosa and Nasal polyps from aspirin tolerant and aspirin intolerant patients with asthma
The Journal of Allergy and Clinical Immunology, 2004Co-Authors: Laura Pujols, Joaquim Mullol, Antoni Xaubet, Jordi Rocaferrer, Isam Alobid, César PicadoAbstract:Background Only dynamic studies can elucidate the discrepancies concerning the expression of the inducible COX-2 gene in inflammatory airway diseases. Objectives To quantify the expression and spontaneous regulation of COX-1 and COX-2 mRNAs in Nasal polyps and Nasal Mucosa by real-time PCR. Methods Nasal polyps were obtained from 16 aspirin-tolerant patients with asthma/rhinitis (ATAR) and 18 aspirin-intolerant patients with asthma/rhinitis (AIAR) undergoing Nasal polypectomy. Nasal Mucosa was obtained from 12 subjects undergoing Nasal corrective surgery. All specimens were cut into 3 pieces. One was immediately snap-frozen in liquid nitrogen, and the remaining 2 were left at room temperature for 30 or 60 minutes before freezing. Data are presented as medians and 25th to 75th percentiles of 10 6 cDNA molecules/μg total RNA. Results Baseline COX-2 mRNA levels were significantly lower in both ATAR (0.45; 0.13-1.20; P P P Conclusion These results suggest differential kinetics of COX-2 mRNA between Nasal Mucosa and Nasal polyps. AIAR Nasal polyps appear to have a greater abnormality of the COX-2 pathway than ATAR.
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Expression of the glucocorticoid receptor alpha and beta isoforms in human Nasal Mucosa and polyp epithelial cells.
Respiratory medicine, 2003Co-Authors: Laura Pujols, Joaquim Mullol, Pedro Benítez, Alfons Torrego, Antoni Xaubet, Josep De Haro, César PicadoAbstract:Abstract The lower sensitivity of the inflamed Nasal Mucosa to glucocorticoids might be related to an increased expression of the glucocorticoid receptor (GR) beta isoform. We investigated GR α and GR β mRNA expression in epithelial cells from Nasal Mucosa and Nasal polyps. GR α mRNA was at least 1000 times more expressed than GR β mRNA in both tissues. GR β expression (mean±SEM of 10 3 cDNA copies/μg of total RNA) was higher in Nasal polyps (1.15±0.19; n =27; P n =32). Nasal polyps with>3% of inflammatory cells had higher GR β levels (1.40±0.29; n =16) than both Nasal Mucosa ( P n =11; P β expression was found between Nasal Mucosa and polyps with ≤ 3% of inflammatory cells. GR β expression correlated with the inflammatory cell number, especially with mast cells ( r =0.50, P α mRNA expression between Nasal Mucosa and Nasal polyps. In summary, GR α is far more expressed than GR β in both tissues. The increased expression of GR β may be related to the presence of inflammatory cells.
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effect of budesonide and nedocromil sodium on il 6 and il 8 release from human Nasal Mucosa and polyp epithelial cells
Respiratory Medicine, 2001Co-Authors: Antoni Xaubet, Laura Pujols, Joaquim Mullol, Jordi Rocaferrer, M Fuentes, M Perez, J M Fabra, César PicadoAbstract:Abstract We investigated the effect of budesonide and nedocromil sodium on the secretion of IL-6 and IL-8 by cultured epithelial cells from healthy Nasal Mucosa and Nasal polyps. Human epithelial cell conditioned media was generated with fetal calf serum (FCS) in the presence or absence of budesonide and/or nedocromil sodium. Budesonide inhibited FCS-induced IL-6 and IL-8 release in a dose-dependent manner. The IC25(25% inhibitory concentration) of budesonide on IL-6 release was higher in Nasal polyp than in Nasal Mucosa epithelial cells (34 n M vs. 200 p M ). The IC25of budesonide on IL-8 release was higher in Nasal Mucosa than in Nasal polyps (145 p M vs. 4 p M ). Nedocromil sodium caused a dose-related inhibitory effect on IL-8 release from Nasal Mucosa (IC25, 207 n M ), while it only had a significant effect in Nasal polyps at 10−5 M . Nedocromil sodium had no effect on IL-6 release. The inhibitory effect of budesonide was higher than that of nedocromil sodium on both Nasal polyps and Nasal Mucosa. Budesonide and nedocromil sodium may exert their anti-inflammatory action in the respiratory Mucosa by modulating the secretion of IL-6 and IL-8. The different effect of budesonide and nedocromil sodium on IL-6 and IL-8 release may be explained by differences in the mechanisms which regulate the upregulation of these cytokines in inflammatory responses.
Noriaki Takeda - One of the best experts on this subject based on the ideXlab platform.
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preseasonal prophylactic treatment with antihistamines suppresses Nasal symptoms and expression of histamine h1 receptor mrna in the Nasal Mucosa of patients with pollinosis
Methods and Findings in Experimental and Clinical Pharmacology, 2010Co-Authors: Hiroyuki Mizuguchi, Hiroyuki Fukui, Yoshiaki Kitamura, Y Kondo, Wakana Kuroda, H Yoshida, Y Miyamoto, Masashi Hattori, Noriaki TakedaAbstract:Administration of antihistamines 2-4 weeks before the pollen season showed a greater inhibitory effect on Nasal allergy symptoms in patients with seasonal allergic rhinitis. However, the mechanism of slow-onset effects of preseasonal treatment with antihistamines remains unclear. Here, we investigated the effect of preseasonal prophylactic treatment with antihistamines on Nasal symptoms and the expression of histamine H, receptor (H1R) mRNA of the Nasal Mucosa in patients with cedar pollen pollinosis. During the peak pollen period, the expression of H7R mRNA in the Nasal Mucosa and the scores of sneezing and watery rhinorrhea in patients receiving preseasonal prophylactic treatment with antihistamines were significantly suppressed in comparison with those in the patients without treatment. Moreover, there was a significant correlation between the Nasal symptoms and the expression of H1R mRNA in both patients with or without preseasonal prophylactic treatment. These findings suggest that preseasonal prophylactic treatment with antihistamines is more effective than on-seasonal administration to patients with pollinosis in reducing Nasal symptoms during the peak pollen period by suppressing H1R gene expression in the Nasal Mucosa.
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preseasonal prophylactic treatment with antihistamines suppresses Nasal symptoms and expression of histamine h receptor mrna in the Nasal Mucosa of patients with pollinosis
Methods and Findings in Experimental and Clinical Pharmacology, 2010Co-Authors: Hiroyuki Mizuguchi, Hiroyuki Fukui, Y Kondo, Wakana Kuroda, H Yoshida, Y Miyamoto, Masashi Hattori, Y Kitamura, Noriaki TakedaAbstract:Administration of antihistamines 2-4 weeks before the pollen season showed a greater inhibitory effect on Nasal allergy symptoms in patients with seasonal allergic rhinitis. However, the mechanism of slow-onset effects of preseasonal treatment with antihistamines remains unclear. Here, we investigated the effect of preseasonal prophylactic treatment with antihistamines on Nasal symptoms and the expression of histamine H, receptor (H1R) mRNA of the Nasal Mucosa in patients with cedar pollen pollinosis. During the peak pollen period, the expression of H7R mRNA in the Nasal Mucosa and the scores of sneezing and watery rhinorrhea in patients receiving preseasonal prophylactic treatment with antihistamines were significantly suppressed in comparison with those in the patients without treatment. Moreover, there was a significant correlation between the Nasal symptoms and the expression of H1R mRNA in both patients with or without preseasonal prophylactic treatment. These findings suggest that preseasonal prophylactic treatment with antihistamines is more effective than on-seasonal administration to patients with pollinosis in reducing Nasal symptoms during the peak pollen period by suppressing H1R gene expression in the Nasal Mucosa.
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effect of glucocorticoid on upregulation of histamine h1 receptor mrna in Nasal Mucosa of rats sensitized by exposure to toluene diisocyanate
Acta Oto-laryngologica, 2004Co-Authors: Yoshiaki Kitamura, Hiroyuki Fukui, Ayako Miyoshi, Y Murata, Bukasa Kalubi, Noriaki TakedaAbstract:Objective —Histamine is a major chemical mediator in the development of Nasal allergy, which is characterized by Nasal hypersensitivity. In this study, we used rats sensitized by exposure to toluene diisocyanate (TDI) as an animal model of Nasal hypersensitivity and examined changes in expression of histamine H1 receptor (H1R) in the Nasal Mucosa. The effect of glucocorticoid on upregulation of H1R in Nasal Mucosa induced by TDI was also examined. Material and Methods —In rats sensitized by exposure to TDI, Nasal allergy-like behavior was scored during a 10-min period after TDI provocation. The expression of H1R in the Nasal Mucosa was determined by means of a real-time quantitative reverse transcriptase polymerase chain reaction and a [3H]mepyramine binding assay. Results —In TDI-sensitized rats, Nasal allergy-like behavior, such as sneezing and watery rhinorrhea, was induced after intraNasal application of TDI and Nasal hypersensitivity to histamine was significantly increased. The level of H1R mRNA exp...
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Nasal Mucosa sensitization with toluene diisocyanate tdi increases preprotachykinin a ppta and preprocgrp mrnas in guinea pig trigeminal ganglion neurons
Brain Research, 1992Co-Authors: Bukasa Kalubi, Satoshi Ogino, Morihiro Irifune, Toru Matsunaga, Noriaki Takeda, Hong Suling, Mariko Yamano, Masaya TohyamaAbstract:Abstract Toluene diisocyanate (TDI) induces respiratory allergy in mammals. Using immunohistochemistry and in situ hybridization histochemistry, the present study examined effects of Nasal Mucosa sensitization by TDI on the immunoreactivity for substance P (SP) and calcitonin gene-related peptide (CGRP) and on the expression of their mRNAs in guinea pig trigeminal ganglion and their terminals. Single intraNasal application of TDI (acute experiment) did not induce Nasal allergy-like behaviours and failed to cause changes of SP and CGRP immunoreactivity and in the expression of preprotachykinin A (PPTA) mRNA and preproCGRP mRNA coding for SP and CGRP respectively in the trigeminal ganglion neurons. However, repeated application of TDI (chronic experiment) caused a dramatic increase of SP and CGRP immunoreactivity in peripheral neurites of sensory nerves in the Nasal Mucosa but a slight increase in the spinal trigeminal nucleus, a decrease of the same immunoreactivities in the cell bodies of the trigeminal ganglion neurons, and an increase of the expression of PPTA and preproCGRP mRNA in the same neurons. These findings suggest that chronic exposure of the Nasal Mucosa to TDI apparently causes enhancement of both the biosynthesis of SP and CGRP and their axonal transport in the trigeminal system.
Hannah J Gould - One of the best experts on this subject based on the ideXlab platform.
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biased use of vh5 ige positive b cells in the Nasal Mucosa in allergic rhinitis
The Journal of Allergy and Clinical Immunology, 2005Co-Authors: Heather A Coker, Graham K Banfield, Victoria A Carr, Stephen R Durham, Helen E Harries, Elfy B Chevretton, Paul Hobby, Brian J Sutton, Hannah J GouldAbstract:Background IgE antibody-producing B cells are enriched in the Nasal Mucosa in patients with allergic rhinitis because of local class switching to IgE. The expressed IgE V H genes also undergo somatic hypermutation in situ to generate clonal families. The antigenic driving force behind these events is unknown. Objective To examine the possible involvement of a superantigen in allergic rhinitis, we compared the variable (V H ) gene use and patterns of somatic mutation in the expressed IgE heavy-chain genes in Nasal biopsy specimens and blood from allergic patients and the IgA V H use in the same biopsy specimens and also those from nonallergic controls. Methods We extracted mRNA from the Nasal biopsy specimens of 13 patients and 4 nonallergic control subjects and PBMCs from 7 allergic patients. IgE and IgA V H regions were RT-PCR amplified, and the DNA sequences were compared with those of control subjects. We constructed a molecular model of V H 5 to locate amino acids of interest. Results We observed a significantly increased frequency of IgE and IgA V H 5 transcripts in the Nasal Mucosa of the allergic patients compared with the normal PBMC repertoire. Within IgE and IgA V H 5 sequences in the Nasal Mucosa, the distribution of replacement amino acids was skewed toward the immunoglobulin framework regions. Three of 4 nonintrinsic hotspots of mutation identified in the V H 5 sequences were in framework region 1. The hotspots and a conserved V H 5-specific framework residue form a tight cluster on the surface of V H 5. Conclusion Our results provide evidence for the activity of a superantigen in the Nasal Mucosa in patients with allergic rhinitis.
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allergen drives class switching to ige in the Nasal Mucosa in allergic rhinitis
Journal of Immunology, 2005Co-Authors: Pooja Takhar, Heather A Coker, S R Durham, Lyn Smurthwaite, David J Fear, Graham K Banfield, Victoria A Carr, Hannah J GouldAbstract:IgE-expressing B cells are over 1000 times more frequent in the Nasal B cell than the peripheral blood B cell population. We have investigated the provenance of these B cells in the Nasal Mucosa in allergic rhinitis. It is generally accepted that expression of activation-induced cytidine deaminase and class switch recombination (CSR) occur in lymphoid tissue, implying that IgE-committed B cells must migrate through the circulation to the Nasal Mucosa. Our detection of mRNA for activation-induced cytidine, multiple germline gene transcripts, and e circle transcripts in the Nasal Mucosa of allergic, in contrast to nonallergic control subjects, however, indicates that local CSR occurs in allergic rhinitis. The germline gene transcripts and e circle transcripts in grass pollen-allergic subjects are up-regulated during the season and also when biopsies from allergic subjects are incubated with the allergen ex vivo. These results demonstrate that allergen stimulates local CSR to IgE, revealing a potential target for topical therapies in allergic rhinitis.
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local somatic hypermutation and class switch recombination in the Nasal Mucosa of allergic rhinitis patients
Journal of Immunology, 2003Co-Authors: Heather A Coker, S R Durham, Hannah J GouldAbstract:Immunoglobulin E is produced by Nasal B cells in response to allergen. We have analyzed IgE VH region sequences expressed in the Nasal Mucosa of patients suffering from allergic rhinitis. VH region sequences were amplified by RT-PCR from IgE+ B cells from Nasal biopsies. In two of six patients, sequence analysis clearly demonstrated the presence of closely related IgE+ B cell clones: cells displaying identical signature regions across CDR3/FWR4, indicating a common clonal ancestry, but a mixture of shared and diverse somatic mutations across the VH region. Furthermore, in one of the two patients exhibiting related IgE+ B cell clones, five IgA+ B cell clones, related to the IgE+ B cell family, were also isolated from the patient’s Nasal Mucosa. This evidence, combined with the local expression of mRNA transcripts encoding activation-induced cytidine deaminase, suggests that local somatic hypermutation, clonal expansion, and class switch recombination occur within the Nasal Mucosa of allergic rhinitics. The presence of related B cells in the Nasal Mucosa does not appear to result from the random migration of IgE+ cells from the systemic pool, as analysis of a nonatopic subject with highly elevated serum IgE did not exhibit any detectable VH-Ce transcripts in the Nasal Mucosa. We have provided evidence that suggests for the first time that the Nasal Mucosa of allergic rhinitics is an active site for local somatic hypermutation, clonal expansion, and class switch recombination, making it of major significance for the targeting of future therapies.
Hiroyuki Fukui - One of the best experts on this subject based on the ideXlab platform.
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preseasonal prophylactic treatment with antihistamines suppresses Nasal symptoms and expression of histamine h1 receptor mrna in the Nasal Mucosa of patients with pollinosis
Methods and Findings in Experimental and Clinical Pharmacology, 2010Co-Authors: Hiroyuki Mizuguchi, Hiroyuki Fukui, Yoshiaki Kitamura, Y Kondo, Wakana Kuroda, H Yoshida, Y Miyamoto, Masashi Hattori, Noriaki TakedaAbstract:Administration of antihistamines 2-4 weeks before the pollen season showed a greater inhibitory effect on Nasal allergy symptoms in patients with seasonal allergic rhinitis. However, the mechanism of slow-onset effects of preseasonal treatment with antihistamines remains unclear. Here, we investigated the effect of preseasonal prophylactic treatment with antihistamines on Nasal symptoms and the expression of histamine H, receptor (H1R) mRNA of the Nasal Mucosa in patients with cedar pollen pollinosis. During the peak pollen period, the expression of H7R mRNA in the Nasal Mucosa and the scores of sneezing and watery rhinorrhea in patients receiving preseasonal prophylactic treatment with antihistamines were significantly suppressed in comparison with those in the patients without treatment. Moreover, there was a significant correlation between the Nasal symptoms and the expression of H1R mRNA in both patients with or without preseasonal prophylactic treatment. These findings suggest that preseasonal prophylactic treatment with antihistamines is more effective than on-seasonal administration to patients with pollinosis in reducing Nasal symptoms during the peak pollen period by suppressing H1R gene expression in the Nasal Mucosa.
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preseasonal prophylactic treatment with antihistamines suppresses Nasal symptoms and expression of histamine h receptor mrna in the Nasal Mucosa of patients with pollinosis
Methods and Findings in Experimental and Clinical Pharmacology, 2010Co-Authors: Hiroyuki Mizuguchi, Hiroyuki Fukui, Y Kondo, Wakana Kuroda, H Yoshida, Y Miyamoto, Masashi Hattori, Y Kitamura, Noriaki TakedaAbstract:Administration of antihistamines 2-4 weeks before the pollen season showed a greater inhibitory effect on Nasal allergy symptoms in patients with seasonal allergic rhinitis. However, the mechanism of slow-onset effects of preseasonal treatment with antihistamines remains unclear. Here, we investigated the effect of preseasonal prophylactic treatment with antihistamines on Nasal symptoms and the expression of histamine H, receptor (H1R) mRNA of the Nasal Mucosa in patients with cedar pollen pollinosis. During the peak pollen period, the expression of H7R mRNA in the Nasal Mucosa and the scores of sneezing and watery rhinorrhea in patients receiving preseasonal prophylactic treatment with antihistamines were significantly suppressed in comparison with those in the patients without treatment. Moreover, there was a significant correlation between the Nasal symptoms and the expression of H1R mRNA in both patients with or without preseasonal prophylactic treatment. These findings suggest that preseasonal prophylactic treatment with antihistamines is more effective than on-seasonal administration to patients with pollinosis in reducing Nasal symptoms during the peak pollen period by suppressing H1R gene expression in the Nasal Mucosa.
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effect of glucocorticoid on upregulation of histamine h1 receptor mrna in Nasal Mucosa of rats sensitized by exposure to toluene diisocyanate
Acta Oto-laryngologica, 2004Co-Authors: Yoshiaki Kitamura, Hiroyuki Fukui, Ayako Miyoshi, Y Murata, Bukasa Kalubi, Noriaki TakedaAbstract:Objective —Histamine is a major chemical mediator in the development of Nasal allergy, which is characterized by Nasal hypersensitivity. In this study, we used rats sensitized by exposure to toluene diisocyanate (TDI) as an animal model of Nasal hypersensitivity and examined changes in expression of histamine H1 receptor (H1R) in the Nasal Mucosa. The effect of glucocorticoid on upregulation of H1R in Nasal Mucosa induced by TDI was also examined. Material and Methods —In rats sensitized by exposure to TDI, Nasal allergy-like behavior was scored during a 10-min period after TDI provocation. The expression of H1R in the Nasal Mucosa was determined by means of a real-time quantitative reverse transcriptase polymerase chain reaction and a [3H]mepyramine binding assay. Results —In TDI-sensitized rats, Nasal allergy-like behavior, such as sneezing and watery rhinorrhea, was induced after intraNasal application of TDI and Nasal hypersensitivity to histamine was significantly increased. The level of H1R mRNA exp...
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histamine content synthesis and degradation in Nasal Mucosa and lung of guinea pigs treated with toluene diisocyanate tdi
Clinical & Experimental Allergy, 1993Co-Authors: Satoshi Ogino, Ikuo Imamura, Morihiro Irifune, Hiroyuki Fukui, Toru MatsunagaAbstract:Summary We have reported the presence of a histamine synthesizing enzyme, histidine decarboxylase (HDC), and histamine degrading enzymes, histamine N-methyltransferase (HMT) and histaminase (diamine oxidase, DAO) in human Nasal Mucosa and the histamine content of the Mucosa. In this study, we demonstrate the influences of the toluene diisocyanate (TDI) treatment on the histamine content and these enzyme activities in guinea-pigs as an animal model of respiratory hypersensitivity. Application of TDI to the Nasal vestibuli induced intense Nasal allergy-like and mild asthma-like responses in TDI-sensitized guinea pigs. Increases in the histamine content and HDC and HMT activities were observed in the Nasal mueosa and lung of TDI-sensitized guinea pigs. No apparent changes in the histaminase activities were observed in either the Nasal Mucosa or the lung. These data suggest that the turnover rate of histamine is increased in the Nasal Mucosa and the lung of guinea pigs with respiratory hypersensitivity.
Antoni Xaubet - One of the best experts on this subject based on the ideXlab platform.
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dynamics of cox 2 in Nasal Mucosa and Nasal polyps from aspirin tolerant and aspirin intolerant patients with asthma
The Journal of Allergy and Clinical Immunology, 2004Co-Authors: Laura Pujols, Joaquim Mullol, Antoni Xaubet, Jordi Rocaferrer, Isam Alobid, César PicadoAbstract:Background Only dynamic studies can elucidate the discrepancies concerning the expression of the inducible COX-2 gene in inflammatory airway diseases. Objectives To quantify the expression and spontaneous regulation of COX-1 and COX-2 mRNAs in Nasal polyps and Nasal Mucosa by real-time PCR. Methods Nasal polyps were obtained from 16 aspirin-tolerant patients with asthma/rhinitis (ATAR) and 18 aspirin-intolerant patients with asthma/rhinitis (AIAR) undergoing Nasal polypectomy. Nasal Mucosa was obtained from 12 subjects undergoing Nasal corrective surgery. All specimens were cut into 3 pieces. One was immediately snap-frozen in liquid nitrogen, and the remaining 2 were left at room temperature for 30 or 60 minutes before freezing. Data are presented as medians and 25th to 75th percentiles of 10 6 cDNA molecules/μg total RNA. Results Baseline COX-2 mRNA levels were significantly lower in both ATAR (0.45; 0.13-1.20; P P P Conclusion These results suggest differential kinetics of COX-2 mRNA between Nasal Mucosa and Nasal polyps. AIAR Nasal polyps appear to have a greater abnormality of the COX-2 pathway than ATAR.
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Expression of the glucocorticoid receptor alpha and beta isoforms in human Nasal Mucosa and polyp epithelial cells.
Respiratory medicine, 2003Co-Authors: Laura Pujols, Joaquim Mullol, Pedro Benítez, Alfons Torrego, Antoni Xaubet, Josep De Haro, César PicadoAbstract:Abstract The lower sensitivity of the inflamed Nasal Mucosa to glucocorticoids might be related to an increased expression of the glucocorticoid receptor (GR) beta isoform. We investigated GR α and GR β mRNA expression in epithelial cells from Nasal Mucosa and Nasal polyps. GR α mRNA was at least 1000 times more expressed than GR β mRNA in both tissues. GR β expression (mean±SEM of 10 3 cDNA copies/μg of total RNA) was higher in Nasal polyps (1.15±0.19; n =27; P n =32). Nasal polyps with>3% of inflammatory cells had higher GR β levels (1.40±0.29; n =16) than both Nasal Mucosa ( P n =11; P β expression was found between Nasal Mucosa and polyps with ≤ 3% of inflammatory cells. GR β expression correlated with the inflammatory cell number, especially with mast cells ( r =0.50, P α mRNA expression between Nasal Mucosa and Nasal polyps. In summary, GR α is far more expressed than GR β in both tissues. The increased expression of GR β may be related to the presence of inflammatory cells.
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effect of budesonide and nedocromil sodium on il 6 and il 8 release from human Nasal Mucosa and polyp epithelial cells
Respiratory Medicine, 2001Co-Authors: Antoni Xaubet, Laura Pujols, Joaquim Mullol, Jordi Rocaferrer, M Fuentes, M Perez, J M Fabra, César PicadoAbstract:Abstract We investigated the effect of budesonide and nedocromil sodium on the secretion of IL-6 and IL-8 by cultured epithelial cells from healthy Nasal Mucosa and Nasal polyps. Human epithelial cell conditioned media was generated with fetal calf serum (FCS) in the presence or absence of budesonide and/or nedocromil sodium. Budesonide inhibited FCS-induced IL-6 and IL-8 release in a dose-dependent manner. The IC25(25% inhibitory concentration) of budesonide on IL-6 release was higher in Nasal polyp than in Nasal Mucosa epithelial cells (34 n M vs. 200 p M ). The IC25of budesonide on IL-8 release was higher in Nasal Mucosa than in Nasal polyps (145 p M vs. 4 p M ). Nedocromil sodium caused a dose-related inhibitory effect on IL-8 release from Nasal Mucosa (IC25, 207 n M ), while it only had a significant effect in Nasal polyps at 10−5 M . Nedocromil sodium had no effect on IL-6 release. The inhibitory effect of budesonide was higher than that of nedocromil sodium on both Nasal polyps and Nasal Mucosa. Budesonide and nedocromil sodium may exert their anti-inflammatory action in the respiratory Mucosa by modulating the secretion of IL-6 and IL-8. The different effect of budesonide and nedocromil sodium on IL-6 and IL-8 release may be explained by differences in the mechanisms which regulate the upregulation of these cytokines in inflammatory responses.
