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PubMedDate not supplied

Decreased connexin 43 expression correlated with eosinophil infiltration in nasal polyps.

BACKGROUND: A nasal polyp usually is characterized by eosinophil infiltration. Eosinophil-fibroblast interaction is an important event of persistent inflammation in airways. We have found abundant connexin 43 (Cx43) expression in subepithelial fibroblasts of nasal mucosa. Thus, we aim to analyze the relationship of Cx43 expression and eosinophil in nasal polyps. METHODS: In 25 nasal polyps and 19 inferior turbinates, indirect immunofluorescent and hematoxylin and eosin staining were performed in adjacent sections. We calculated the density of Cx43 staining and eosinophil individually by fluorescent and light microscope. RESULTS: Positive Cx43 staining under confocal microscope was shown as punctated spots on cell margin. The density of Cx43 and eosinophil staining was significantly different between groups of inferior turbinate and nasal polyp (p = 0.01 and 0.03, respectively). Decreased Cx43 expression in the subepithelial fibroblast was correlated with eosinophil infiltration in nasal polyps. Spearman rank order coefficient was equal to -0.43 (p < 0.05). CONCLUSION: This is the first demonstration of decreased Cx43 expression related to eosinophil infiltration. To the best of our knowledge, interleukin-8 may be a link between Cx43 and eosinophil and orchestrating both in developing nasal polyps.

Adolescent↗
PubMed1979

Woakes' syndrome: the problems of infantile nasal polyps.

Usually, nasal polyposis in early childhood (children aged less than 5 years) is caused by cystic fibrosis of Kartagener's syndrome. In later age groups, recurrent sinus infections, allergy and ASA disease (asthma, aspirin intolerance and nasal polyps) have to be taken into consideration. Four cases of early childhood polyposis are reported which fit into none of these etiological groups. This newly defined Woakes' syndrome comprises recurrent nasal polyposis with broadening of the nose, frontal sinus aplasia, bronchiectasis, and dyscrinia (production of highly viscous mucus). The disease seems to be hereditary. The possible origins of the disease are discussed.

Bronchiectasis↗
PubMed1984

Free histamine in nasal polyp fluid.

Nasal polyp fluid was extracted from 52 patients to evaluate histamine levels and compare them with the corresponding serum levels. Large but variable amounts of histamine were found in polyp fluid (124-7600 ng/ml) which was between twenty and a thousand times the serum level. There was no significant difference between the polyp histamine levels in patients with a history of asthma, aspirin hypersensitivity, hay fever and positive skin tests.

Aspirin↗
PubMed1993

Mast cell quantitation in nasal polyps, sinus mucosa and nasal turbinate mucosa.

The distribution and abundance of mast cells in nasal polyps, the maxillary sinus mucosa of patients with sinusitis and the turbinate mucosa of allergic rhinitis was microscopically examined using different methods of fixation. In the epithelium of the surface and the ducts of nasal polyps (n = 8), the mean number of mast cells was over 20,000 per mm3 using Mota's fixation and the increase was correlated with the epithelial thickness (P < 0.05). On the other hand those of the maxillary sinus mucosa (n = 6) and the nasal turbinate mucosa (n = 7) were less than 6,000 per mm3. In the subepithelial layer or areas deeper than the area with the glands, however, mast cell counts were less than 3,200 per mm3 in all diseases. More than 70-90 per cent of all mast cells in the epithelium of the mucosal surface and the ducts of the polyp, the maxillary sinus mucosa and nasal turbinates were formalin sensitive. Most of the mast cells in the subepithelial and deeper areas were formalin resistant in all diseases. These results suggest that conditions for mast cell growth differ between polyps and the other diseases, and that the conditions which affect mast cells may contribute to polyp development.

Adolescent↗
PubMed1987

Comparison of arachidonic acid metabolism in nasal polyps and eosinophils.

Nasal polyp tissue is characterized by its frequent infiltration by large numbers of eosinophils. We have studied the metabolism of 14C-labeled arachidonic acid by both nasal polyp tissue and by eosinophils. The major metabolite produced by both is 15-hydroxyeicosatetraenoic acid (HETE) with lesser amounts of 12-HETE. No cyclooxygenase pathway products were found. The 15-lipoxygenase activity of nasal polyps averages 30 times that of normal nasal mucosa or chronically inflamed sinus mucosa. Nasal polyps which contained significant numbers of eosinophils averaged 7 times the 15-lipoxygenase activity of nasal polyps without eosinophilia. Thus, eosinophils appear to be a major source of 15-lipoxygenase activity in nasal polyps.

Arachidonic Acid↗
PubMed1995

Phenol sulfotransferase activities and localization in human nasal polyp epithelium.

Nasal polyp epithelia, which exhibit a wide variation in epithelial cell morphologies, were tested for phenol sulfotransferase (PST) enzymes. Immunohistology revealed little or no detectable PST antigen in normal ciliated pseudostratified epithelia or in simple squamous metaplastic epithelia; however, intense expression was observed in regions of non-ciliated epithelial cell hyperplasia and in squamous epithelial cells overlying such hyperplastic sites. Western blots confirmed the presence of both P-PST (32 kDa) and M-PST (34 kDa) in the tissue extracts. Bimodal distribution of PST activity as a function of 4-nitrophenol concentration was consistent with expression of these two PST isoforms. These results indicate dynamic and epithelial differentiation-dependent expression of human PSTs in the nasal mucosa and suggest that these sulfotransferases can be modulated within human airways in vivo.

Arylsulfotransferase↗
PubMed1995

Site of origin of nasal polyps. Transcranially removed naso-ethmoidal blocks as a screening method for nasal polyps in autopsy material.

In autopsy material naso-ethmoidal blocks were removed in 19 patients. None of the patients had a preceding rhinoscopy. Before removal, the maxillary and sphenoidal sinuses were opened and screened for polyps. After removal the total naso-ethmoidal complex was carefully examined for nasal polyps. The site of origin of the individual polyp was registered and documented photographically. Nine polyps were found in five patients, of which four had no history of asthma, allergy or sinusitis. Two patients had unilateral solitary polyps, three had polyps bilaterally. All polyps were found in the meatus. Eighty-nine per cent of the polyps were related to the clefts from the ethmoid. Polyps were not observed inside the ethmoidal and other paranasal sinuses.

Aged↗
PubMed2006

[Etiology of nasal polyps: an update].

Nasal polyps are the results of chronic inflammation of nasal mucosa. Ethiopathology of nasal polyposis is still unclear and investigated. The main aim of this study was the assessment of interleukin 2 (IL-2), 4 (IL-4) and 13 (IL-13) and interferon gamma (IFN-gamma) expressions in two groups of patients with nasal polyps: non-allergic and allergic to dust. Twelve patients with nasal polyposis were selected, six of them allergic and six non-allergic. Patients with allergy were distinguished from those without allergy on the basis of positive allergy skin tests to dust and serum levels of IgE. Blood sample was obtained from patients and examined for the expression of Interleukin 2, 4, and 13 and IFN-gamma by intracellular staining procedure after stimulation with PMA/ionomycin (phorbol 12-myristate 13-acetate) and allergen (D. pteronyssimus, Allergopharma). Negative correlation was found between expression of Interleukin 2, 4, 13 after PMA/ionomycin and allergen stimulation (p > 0.05) into two groups. Although mean expression of IFN-gamma and IL-2 were lower in allergic patients with nasal polyps. Mean value of IL-4 and IL-13 were higher in allergic patients in comparison to non-allergic, but the correlations were not significant. We did not find correlations between expression of investigated interleukins and bronchial asthma and ASA-intolerance existed in patients (p > 0.05). We found that expression of IFN-gamma was significantly lower in patients with polyps recurrences followed by polypectiomies (p = 0.05). In patients who used intranasal local steroid before treatment we observed significant decrease of 11-2 and 11-13 levels after allergen stimulation (p = 0.,034, p = 0.023). No specific differences of expression of investigated cytokines between allergic versus non-allergic patients suggests that the allergic mechanism may not play an fundamental role in the aetiology and formation of nasal polyps. Furthermore local steroids seem to be used in every patient after polypectomy because of their anti-inflammatory stimulation.

Adult↗
PubMedDate not supplied

Macrolide treatment decreased the size of nasal polyps and IL-8 levels in nasal lavage.

Recently, epidemiologic and experimental studies have been reported that long-term macrolides are effective for the treatment of chronic airway inflammatory diseases including diffuse panbronchiolitis, chronic rhinosinusitis, and cystic fibrosis (Jaffe A, Francis J, Rosenthal M, et al. Long-term azithromycin may improve lung function in children with cystic fibrosis. Lancet 351:420, 1998), and that macrolides can directly reduce the production of IL-8 by nasal epithelial cells (Suzuki H, Shimomura A, Ikeda K, et al. Inhibitory effect of macrolides on interleukin-8 secretion from cultured human nasal epithelial cells. Laryngoscope 107:1661-1666, 1997). In this study we administered macrolides with 14-membered rings to patients with nasal polyps due to chronic rhinosinusitis for at least 3 months and measured the IL-8 level in nasal lavage from those patients. The IL-8 levels in nasal lavage from patients with nasal polyps were reduced during macrolide treatment. There was significant correlation between decreased IL-8 levels in nasal lavage and the clinical effect of macrolides on the size of the nasal polyps. In the group whose polyps were reduced in size, the IL-8 levels dramatically decreased from 231.2 pg/mL to 44.0 pg/mL (p < 0.05), and were significantly higher before macrolide treatment than those in the group whose polyps showed no change (p < 0.005). This reduction in IL-8 may be an important aspect of the effect of macrolide treatment on nasal polyps in chronic rhinosinusitis.

Anti-Bacterial Agents↗
PubMed1996

[Estradiol receptors expression in nasal polyps and its significance].

Nasal polyps are generally considered as a result of extreme nasal mucosal edema induced by long-term recurrent inflammation of the respiratory mucosa. The estradiol (E2) has been demonstrated to play a facilitating role in nasal inflammation. To evaluate the effect of estradiol on the pathogenesis of nasal polyps, the expression of E2 receptors in paraffin section from patients with nasal polyps (84 cases), chronic hypertrophic rhinitis (6 cases) and healthy control subjects were investigated by means of immunohistochemistry for E2 receptors and toluidine blue staining for mast cells. It was shown that there was high expression of E2 receptors in 61 out of 84 cases (male 40, female 44) of nasal polyps and the expression distributed equally among both sexes. Low expression of E2 receptors presents in 2 out of 6 cases of chronic rhinitis and 1 out of 4 healthy subjects. Noteworthily, the E2 receptor expressing cells are similar with the mast cells in shape and distribution. The authors speculate that they may be identical cells. E2 receptor expression in nasal polyps suggests that estradiol plays certain role in the development of nasal polyps.

Adult↗
PubMed1992

[Studies on the function of mast cells infiltrating in nasal polyps].

The function of nasal polyp mast cells has not been elucidated despite the large number of these cells observed in tissues. We examined these mast cells histochemically, immunohistologically and functionally. Ninety-three percent of collagenase dispersed cells in a nasal polyp were formalin-sensitive. These dispersed cells released histamine in reaction to calcium ionophore A23187 in a dose dependent manner, but not in response to C5a, Compound 48/80 or Substance P. From these results, dispersed mast cells from nasal polyps were considered to be analogous to dispersed mast cells from the human lung and nasal mucosa but not those from human skin. On the other hand, in the reaction with anti-human IgE, dispersed mast cells from a non allergic nasal polyp could not be seen to release histamine. In only 2 of 7 patients, could histamine release in response to Japanese red cedar antigen, from mast cells sensitized passively with the serum of Japanese red cedar pollinosis, seen. Using small tissue samples from polyps, histamine was released by anti-human IgE in allergic patients but not in non allergic patients. Immunohistologically in allergic nasal polyps, some IgE positive mast cells could be seen, whereas in non allergic polyps these cells were absent. These observations suggest that mast cells which had accumulated in nasal polyps both with and without allergy were capable of functional histamine release, whereas in the nasal polyps of allergy patients but not in non-allergic patients these cells are involved in IgE mediated reactions.

Adolescent↗
PubMed2006

Endothelial and epithelial expression of eotaxin-2 (CCL24) in nasal polyps.

BACKGROUND: Nasal polyposis is mostly associated with eosinophilia of mucosal tissue. This points to the implication of CC chemokines in nasal eosinophilia. Recently the CC chemokine eotaxin-2 (CCL24) was identified. This study was initiated to localize the cellular source, analyze expression of mRNA, and quantify protein synthesis of CCL24. METHODS: Specimens of nasal inferior turbinates from controls and polypous tissue from patients suffering from chronic polypous sinusitis were collected. Furthermore, fibroblasts and epithelial cells were cultured. CCL24 protein was analyzed by immunohistochemistry and ELISA, expression of mRNA by SQ-RT-PCR. RESULTS: CCL24 was observed in endothelial and epithelial cells. Specimens from patients expressed significantly (>2fold) more CCL24 mRNA than controls. Fibroblasts and unstimulated cells did not express CCL24 mRNA. Upon stimulation with TNF-alpha, INF-gamma, IL-4, or costimulation with TNF-alpha and INF-gamma CCL24 mRNA was significantly enhanced (3.2-19.6%). In controls, fibroblast, and unstimulated cells CCL24 protein was below detection limit. Most polyps comprised significant amounts of CCL24 (mean 0.24 ng/mg). TNF-alpha, INF-gamma or IL-4 induced CCL24 protein (0.1-0.3 ng/ml) in epithelial cells. Costimulation with TNF-alpha and IL-4 (0.1-30 and 1-30 ng/ml, respectively) synergistically induced synthesis of CCL24 protein (0.18-0.31 ng/ml). CONCLUSION: In nasal polyps endothelial and epithelial cells are obviously the main source of CCL24, which was shown for transcription (mRNA) and production (protein) levels and was associated with diseases. Results gave evidence of CLL24- directed migration of cells from inside (the bloodstream) to the epithelial side (mucosa) in eosinophilic inflammatory diseases, e.g. nasal polyposis.

Adolescent↗
PubMed2000

Inhibition of GM-CSF secretion by topical corticosteroids and nedocromil sodium. A comparison study using nasal polyp epithelial cells.

Nasal epithelial cells maintain eosinophil survival by secreting granulocyte/macrophage colony-stimulating factor (GM-CSF). Corticosteroids antagonize eosinophil viability induced by GM-CSF. We investigated the effect of topical corticosteroids and nedocromil sodium on the release of GM-CSF from nasal polyp epithelial cells. Epithelial cells were obtained from 19 patients undergoing nasal polypectomy and cultured. After reaching confluence, cultured cells were stimulated with 10% foetal calf serum in the absence and presence of four topical corticosteroids and nedocromil sodium for 48 h. GM-CSF was measured by enzyme linked immunosorbent assay (ELISA). Fluticasone propionate was the most potent inhibitor of GM-CSF release (IC25 = 46 pM) closely followed by budesonide (IC25 = 4 nM), beclomethasone dipropionate (IC25 = 40 nM) and triamcinolone acetonide (IC25 = 75 nM). Nedocromil sodium had no effect on GM-CSF release. We conclude that the effect of topical steroids on reducing eosinophil infiltration in nasal polyps may be due in part to downregulation, among other cytokines, of epithelial GM-CSF production which prolongs eosinophil viability. Quantitatively, fluticasone propionate inhibited GM-CSF production more potently than budesonide, beclomethasone dipropionate and triamcinolone acetonide.

Administration, Topical↗
PubMedDate not supplied

Nasal polyps and immunoglobulin E (IgE).

Nasal polyps are usually found in nonallergic individuals. However, when nasal polyps and atopy occur together, a special interaction exists. Total and specific immunoglobulin E (IgE) are found in significantly greater concentration in nasal polyp tissue than in serum and tonsil tissue. Immunoglobulin A (IgA) is also more concentrated in nasal polyps than serum. Patients with nasal polyps and allergies seem to have a greater recurrence rate after surgical polypectomy. Frequently, polyp recurrence occurs during specific pollen seasons in sensitive individuals. Upper respiratory infections are also a precipitating factor for recurrence. Nasal ciliary beat frequency is inhibited in patients with chronic sinusitis, allergic nasal reactions, and nonspecific nasal eosinophilia syndromes: nonallergic rhinitis with eosinophils (NARES) and blood eosinophilic nonallergic rhinitis (BENARS). Nasal polyps are frequently associated with these conditions, which may predispose the nasal mucosa to infections and increased risk for developing nasal polyps. When nasal polyps and allergies occur together, it is important to treat the allergic condition. This takes the form of identifying the allergens, eliminating them from the environment (if possible) using antihistamines/decongestants, and nasal antiinflammatory drugs such as topical steroids. Hyposensitization may be considered in resistant cases.

Humans↗
PubMed1996

Mucociliary function in patients with nasal polyps.

Patients with nasal polyposis complain of nasal blockage and rhinorrhoea, which may be due to impaired mucociliary clearance. The saccharine clearance time and ciliary beat frequency of samples of ciliated epithelium from patients with nasal polyps was measured. We also studied the effect of fluid from the oedematous stroma of nasal polyps and of histamine and prostaglandin (PG) D2, E2 and F2 alpha on the cilia from normal individuals. Polyp fluid was found to increase ciliary beat frequency. Histamine and PGD2 had no effect, but PGE2 and PGF2 alpha both increased ciliary beat frequency and so may cause the ciliostimulatory effect of polyp fluid. The saccharine clearance time was prolonged in three of nine patients, but ciliary beat frequency was only slightly reduced in one of these. Thus, where mucociliary clearance is reduced, it is likely to be due to abnormalities of mucus rather than impaired ciliary activity.

Cilia↗
PubMed2005

Regulation of expression of galectin-7 in human nasal polyps by budesonide.

BACKGROUND: Nasal polyposis is a model for the study of inflammatory processes. We analyzed the expression of galectin-7, a growth regulator, in surface epithelium, glandular epithelium, and connective tissue in human nasal polyps, and examined the effect of the glucocorticoid budesonide on its expression in human nasal polyps ex vivo. METHODS: Using quantitative, computer-assisted microscopy and immunohistochemistry, we measured galectin-7 expression in nine nasal polyps obtained by surgical resection. Five polyps came from allergic patients and four came from non-allergic patients. RESULTS: Galectin-7 was expressed in all three polyp tissues analyzed. Treatment of polyps from allergic and non-allergic patients with 50 ng/ml budesonide increased the extent of galectin-7 expression in the connective tissue (p = 0.01). Conversely, budesonide at this concentration did not apparently affect galectin-7 expression in glandular epithelium; only a slight decrease in the percentage of the galectin-7-immunopositive cells was observed. In the surface epithelium of nasal polyps from non-allergic patients, the percentage of galectin-7-immunopositive cells was decreased (p = 0.03) by treatment with 250 ng/ml budesonide. In nasal polyps from allergic patients, this percentage was increased by treatment with 50 ng/ml budesonide (p = 0.0001). CONCLUSIONS: These data are consistent with a role for galectin-7 in the regulation of cell growth through a pro-apoptotic effect. Galectin-7 expression coincides with the degree of epithelial stratification, and is subject to upregulation in the connective tissue in response to treatment with 50 ng/ml budesonide. Budesonide modulates galectin-7 expression differently in the surface epithelia of polyps from allergic and non-allergic patients.

Anti-Inflammatory Agents↗
PubMed1994

Lymphocyte subsets and antigen-specific IgE antibody in nasal polyps.

We tried to elucidate the role of allergic factors in the pathogenesis of nasal polyps. Nasal polyps were obtained from 22 patients with chronic sinusitis which included eight patients proved to have nasal allergy by history, skin test, and serum-specific IgE against houst dust mite. Immunohistochemical studies of lymphocyte subpopulations in the mucosa of nasal polyps were performed with monoclonal antibodies, and the concentrations of antigen-specific IgE in nasal polyps were measured by the fluoroallergosorbent test. In the epithelium, few HLA-DR+ cells were constantly present. In the submucosa, pan T cell marker CD2 was detected more often than CD19 (B cell), and more CD8 (T suppressor/cytotoxic) cells than CD4 (T helper/inducer) cells were found. IgE-producing plasma cells were rarely present. The lymphocyte subpopulations and the levels of antigen-specific IgE in nasal polyps were not different between the allergic and nonallergic groups. This suggests that allergy may not be the cause, and cellular immunity of antigen presenting cells and T lymphocytes, which consecutively induce infiltration and degranulation of mast cells by the production of cytokines, may be involved in the formation of nasal polyps with sinusitis.

Adolescent↗
PubMed2001

Expression of transforming growth factor-beta 1 and alpha-smooth muscle actin of myofibroblast in the pathogenesis of nasal polyps.

The pathophysiology of nasal polyps remains unclear, but recent work suggests that many cytokines are produced in nasal polyps (NPs) and that they may play various important roles in the pathogenesis of NPs. Transforming growth factor-beta 1 (TGF-beta 1), secreted by many inflammatory cells, is a potent inducer of myofibroblasts. Myofibroblasts express alpha-smooth muscle actin (alpha-SMA) and a source of extracellular matrix (ECM). In this study, we investigated a potential link between inflammation and the growth process in human NPs. Sixteen patients who were affected by NPs and who had undergone functional endoscopic sinus surgery were included in this study. Nasal mucosa of inferior turbinate (NM) of 10 patients who had received rhinoplasty or turbinectomy for other disease was used as the control. alpha-SMA and TGF-beta 1 were detected using immunohistochemistry and the number of labeled cells were counted (alpha-SMA and TGF-beta 1 indices). The expression of alpha-SMA and TGF-beta 1 indices found in NPs and NM was compared using Student's t-test. In our study, alpha-SMA and TGF-beta 1 indices were found to be significantly higher in nasal polyps than in nasal mucosa. TGF-beta 1 produced by inflammatory cells can influence the development of myofibroblasts which in turn can induce extracellular matrix accumulation and, therefore, TGF-beta 1 plays a important role in the formation of nasal polyps.

Actins↗