The acid mucopolysaccharide and collagen content of human nasal polyps, human and animal nasal mucosa.
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Dynamics of COX-2 in nasal mucosa and nasal polyps from aspirin-tolerant and aspirin-intolerant patients with asthma.
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/microg total RNA. RESULTS: Baseline COX-2 mRNA levels were significantly lower in both ATAR (0.45; 0.13-1.20; P <.05) and AIAR (0.24; 0.12-0.41; P <.001) nasal polyps than in nasal mucosa (1.35; 0.52-3.90). COX-2 mRNA expression did not change over time in nasal mucosa but increased significantly in ATAR nasal polyps ( P <.05), reaching similar levels to nasal mucosa after 60 minutes. In contrast, COX-2 mRNA showed no significant change over time in AIAR nasal polyps. COX-1 mRNA was higher in nasal polyps than in nasal mucosa, and its expression was not modified over time in any group of patients. 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.
Adult↗
[Expression of CD68 CD45RO CD20 and proliferating cell nuclear antigen in nasal polyps].
OBJECTIVE: To study the cellular expression of CD45RO, CD20, CD68 and proliferating cell nuclear antigen (PCNA) in nasal polyps. METHODS: Nasal polyp tissues from 50 patients were evaluated for cellular expression of CD45RO, CD20, CD68 and PCNA using immunohistochemistry SP by counting the average number in 5 chosen high-power fields, Histopathological observations were combined with HE. Analyses were performed on SPSS10.0. RESULTS: CD68+ cells were expressed more in nasal polyps dominated by eosinophils than by neutrophils(P < 0.05). There was no difference between CD45RO and CD20, but both of them had negative correlation(P = 0.05). Significant correlation was found between CD68+ cells and eosinophils or PCNA positive cells on epithelium. PCNA positive cells on epithelium had significant correlation on fibroblast (P < 0.05). CONCLUSION: Inflammatory cell infiltration (eosinophilia CD45RO, CD20, CD68) and cell proliferating in epithelium cells, glandular cell and fibroblast are strongly correlated with formation of nasal polyps. The nasal polyps are not only characteristic of eosinophilia but also by lymphocytes dominated by CD45RO and CD68 positive cells. CD68 may be stem cell of nasal polyp.
Antigens, CD↗
[Significance and expression of transforming growth factor beta in human nasal polyp tissue].
OBJECTIVE: To explore the pathogenesis of nasal polyposis and the expression of transforming growth factor beta (TGF-beta) in human inflammatory nasal polyps. METHODS: TGF-beta 1-3 in nasal polyp tissues and inferior turbinate mucosa of twenty-five polyposis patients were detected with immunohistochemistry alkaline phosphatase and anti-alkaline phosphatase (APAAP) method. The inferior turbinate mucosa of eight healthy volunteers were selected as control. Six polyp tissues were estimated with double immunolabeling and Western-blot analysis to compare the characterization of the TGF-beta isoforms expression and the proportion of macrophages and eosinophils in nasal polyp tissues. RESULTS: The expression of TGF-beta 1-3 in nasal polyps was significantly higher than that in nasal mucosa and indetecable in nasal mucosa from healthy volunteers; TGF-beta 1 was the main isoform detected in nasal polyps; TGF-beta positively was accompanied by numerous macrophage and eosinophil infiltration. CONCLUSIONS: TGF-beta mainly TGF-beta 1 is strongly expressed in nasal polyps and its mucosa, where it could be produced by macrophages and eosinophils. TGF-beta could induce modification of epithelium and connective tissue and therefore be involved in the pathogenesis of nasal polyposis.
Eosinophils↗
[Expression of nitric oxide synthase and its significance in nasal polyps].
OBJECTIVE: To study the expression of nitric oxide synthase (NOS) and its activity in nasal polyps and its significance. METHOD: Septectomy and immunohistochemisty were used to examine NOS activity and identify the expression of inducible NOS (iNOS) and endotheial NOS (eNOS) in human nasal specimens from patients undergoing nasal spectrumtomy (n = 20) or nasal polypectomy (n = 30). RESULT: The activity of NOS was significantly higher in nasal polyps than in nasal mucosa (4.079 +/- 0.655) U/Pro vs (1.526 +/- 0.310) U/Pro (P<0.01). iNOS reaction product was located in epithelial cells, vascular endothelial cells, nasal glands and inflammation cells of nasal polyps. iNOS reaction product almost was not be founded in nasal mucosa. Amount of. iNOS positive cells in nasal polyps was higher than in nasal mucosa (P<0.01). eNOS reaction product were located in nasal polyps and nasal mucosa. There was no quantitative difference of eNOS between in nasal polyps and nasal mucosa. Amount of iNOS positive cells was significantly higher than of eNOS positive cells in nasal polyps (P<0.01). CONCLUSION: iNOS, mainly expressed in nasal polyps, locates in epithelial cells and vascular endothelial cells and nasal glands and inflammation cells in nasal polyps, which produce NO at high concentration that plays an important role in the formation of nasal polyps.
Adult↗
[Nasal polyps is not a homogenous pathology].
UNLABELLED: Nasal polyposis is still a disease of unknown etiology. Looking at its clinical course it seems to be not homogenous pathology. Inflammation of the mucosa, mainly eosinophilic is probably the most important factor, which leads to the development of nasal polyps. THE AIM OF STUDY: To analyze and compare the history data and eosinophilic inflammation parameters in patients with nasal polyps. MATERIAL AND METHODS: 67 patients with nasal polyposis were included into the study. They were divided into three groups: PP-primary nasal polyps (n = 33-49.2%); A-polyps and bronchial asthma without aspirin intolerance (n = 19-28.4%); ASA-polyps and aspirin-induced asthma (n = 15-22.4%). The history data were taken using patient's questionnaire. To assess the eosinophilic inflammation intensity the blood and nasal eosinophilia and serum eosinophilic cationic protein (ECP) concentration were measured. RESULTS: The average age of all patients was 55 +/- 1.5 (range 32-76), the age distribution was comparable in all groups. The ratio males:females--1.5:1 (PP--2.7:1; A--1.1:1; ASA--0.7:1. The females with nasal polyps much more often suffer from asthma than males (p = 0.036). The age when polyps were first seen was 45.1. The duration of nasal polyps was 10 +/- 10 years (range 0.5-30 years): PP-- 10 +/- 9; A-- 14 +/- 11; ASA-- 7 +/- 7 (A/ASA-- p = 0.045). Period of 6.6 years of rhinitis had preceded the diagnosis of nasal polyposis (PP--7.3; A--7.1; ASA--4.5). Age when asthma was developed (A+ASA groups)--45.5; the duration of asthma was 11 +/- 9 years. 58% of patients had polypectomy/ethmoidectomy (PP--45%; A--60%; ASA--80%). The number of operations per one patient: 1.3 (PP--1.0; A--1.2; ASA--2.0), the most often performed in ASA group (PP/ASA-- p = 0.01 and A/ASA-- p =0.045). The mean interval between polypectomies in all patients--9.1 years (PP--10; A--12, ASA--3.5). Blood eosinophilia: 5.6 +/- 0.4% (PP-- 4.6 +/- 0.5; A-- 6.2 +/- 0.9; ASA-- 7.2 +/- 0.9% and PP/ASA-- p = 0.019; PP/A+ASA-- p = 0.03). Nasal eosinophilia: 18.5 +/- 3% (PP-- 15.0 +/- 4; A-- 15.5 +/- 6; ASA-- 30.0 +/- 8% and PP/ASA-- p = 0.01; A/ASA-- p = 0.02). Serum ECP concentration: 24 +/- 2 microg/l. CONCLUSIONS: The patient's history and the intensity of eosinophilic inflammation are not similar in all nasal polyposis patients, that support the classification into PP, A and ASA groups. The most severe clinical picture and the highest values of eosinophilic parameters are observed in ASA group. Aspirin intolerance seems to be unfavourable prognostic factor in nasal polyposis.
Adult↗
Analysis of gene expression profiles of normal human nasal mucosa and nasal polyp tissues by SAGE.
BACKGROUND: A systemic determination of gene expression profiles in nasal polyp compared with normal nasal mucosa would contribute considerably to the investigation of the disease marker in various rhinopathy and general knowledge on the formation of human nasal polyp. OBJECTIVE: The aim of this study was to identify the transcriptome of the normal human nasal mucosa and nasal polyp by the serial analysis of gene expression. METHODS: mRNA was extracted from normal inferior turbinate mucosa and nasal polyp. Short sequences (tags), each one usually corresponding to a distinct transcript, was isolated and concatemerized into long DNA molecules, which were cloned and sequenced. RESULTS: We detected 65,305 tags for normal nasal mucosa and 55,829 tags for nasal polyp, representing 20,629 and 17,636 potential transcripts species, respectively. Of the unique tags encountered more than once, 92% (normal nasal mucosa) and 90% (nasal polyp) matched known genes or expressed sequence tags, whereas the remainder did not match any GenBank sequences. Therefore, 504 and 539 novel transcripts were identified in normal nasal mucosa and nasal polyp, respectively. Although the expression levels of most transcripts in both libraries were similar, 114 transcripts were differentially expressed at a statistically significant level (P < .05)-that is, 65 and 49 transcripts among them were expressed at a higher level in normal nasal mucosa and nasal polyp, respectively. CONCLUSION: This information should be very useful for basic knowledge as well as for future studies on pathophysiological conditions of human nasal mucosa, providing some clues to evaluate the altered factors in a variety of rhinopathies. CLINICAL IMPLICATIONS: The results of this study might contribute to general knowledge on the formation of human nasal polyp.
Adult↗
[Vascular cell adhesion molecule-1, eotaxin and vascular endothelial growth factor in nasal polyps after endoscopic surgery].
OBJECTIVE: To study the different expression of VCAM-1, eotaxin and VEGF in nasal polyp tissues and in the nasal mucosa of the operative cavity after endoscopic surgery and its significance. METHODS: Paraffin sections of nasal polyps and the nasal mucosa of the operative cavity were studied with immunohistochemical technique and HE staining. RESULTS: (1) Abundant eosinophils were observed in the nasal polyps, however, it was rarely seen in the nasal mucosa of the operative cavity (t = 2.891, P <0.05). (2) The positive expression of VCAM-1 and eotaxin was in nasal polyps and nasal mucosa of operative cavity, and both of the positive area were not statistically significant (t = - 2.051, P > 0.05), but their average density of light was decreased in the nasal mucosa of the operative cavity (t = 3.670, P = 0.05). The positive glandular of eotaxin were increased after endoscopic surgery (t = -2.899, P < 0.05). (3) Expression of VEGF was similar in both groups (t = - 0.037, 0.825, P > 0.05, respectively). CONCLUSIONS: (1) It is suggested that the nasal mucosa of the operative cavity was different from the nasal polyps. (2) The positive expression of VCAM-1 and eotaxin in the nasal mucosa of the operative cavity after endoscopic surgery indicates that eotaxin may up-regulate the expression of VCAM-1 in vessel endothelium and promote adhesion and migration of eosinophils, as a result, to lead to the recurrence of nasal polyps. The glandulous expression of eotaxin may play a key role in the early stage. (3) The expression of VEGF in nasal mucosa after surgery may contribute to the growth of blood vessel and induce increasing of vascular permeability and tissue edema. This may be an important factor in the process of nasal polyp recurrence.
Adolescent↗
Aspirin-induced asthma and nasal polyps.
Asthma, aspirin intolerance and nasal polyps form a triad of aspirin-induced asthma (AIA). Eighteen cases, 6 males and 12 females, who complained of asthma attacks and/or rhinorrhea after ingestion of non-steroidal anti-inflammatory drugs were encountered over several years. The mean age of onset was 32.1 for asthma and 25.4 for rhinitis. Asthma was found in all of the 18 cases and nasal polyps in 13 cases (72.2%). The polyps were recurrent and 7 patients had undergone polypectomies. Urticaria was seen in 44.4% and sinusitis diagnosed by X-ray in 81.8%. Sensitivity to at least one allergen was found in 7 out of 9 cases (77.8%) and 6 out of 11 cases (54.5%) gave results positive for RAST. Eosinophilia was seen in 14 out of 16 patients (87.5%). The pathogenesis of AIA is obscure but is probably related to inhibition of prostaglandin biosynthesis. We concluded that AIA is not a rare disease in Japan either, and the studies for eosinophilia may be useful for elucidation of the pathogenesis of AIA and nasal polyps.
Adult↗
Effect of macrolides on the expression of HLA-DR and costimulatory molecules on antigen-presenting cells in nasal polyps.
To clarify the basis of macrolide therapy for improvement of chronic sinusitis, we investigated the effect of macrolides on the expression of HLA-DR and costimulatory molecules such as CD54 and CD80 on macrophages in nasal polyps. Nasal polyps taken from 54 patients who had or had not been treated with macrolides were immunohistochemically studied. The percentages of CD68-positive macrophages expressing HLA-DR or CD54 were not significantly different between patients treated with macrolides and those not treated with macrolides. However, among patients exhibiting no atopic predisposition, the number of CD80-positive macrophages was higher in patients treated with macrolides than in those not treated. In addition, the percentage of CD80-positive macrophages was negatively correlated with the percentage of infiltrating eosinophils in the polyps. These results demonstrate that macrophages act as antigen-presenting cells, expressing both major histocompatibility complex II and costimulators, and that the expression of CD80 may play a key role in the immune responses occurring in a nasal polyp. Macrolides may modulate the mucosal immune responses through CD80 expression.
Adolescent↗
[Detection of Helicobacter pylori in nasal polyps specimens using urease test GUT plus].
In patients with nasal polyps the colonisation of nasal polyps tissues by Helicobacter pylori was investigated using urease test (GUT plus). In this prospective clinical trials we enrolled 61 subjects who had undergone endoscopic nasal polyps surgery and 30 subjects who had undergone septoplasty (control group) were questioned and biopsy specimens of the removed polyps or the mucosal part of inferior turbinate were tested by the urease test GUT plus. In result Helicobacter pylori was not found in the nasal polyps and mucosal part of inferior turbinate tissue of any of patients including the 43 of 61 patients with nasal polyps and 7 of 30 patients with septum deviation who had symptoms of gastroesophageal reflux. In our study using the urease test GUT plus we were not able to confirm presence of Helicobacter pylori in the nasal polyps tissue. However, further epidemiologic studies using different diagnostic methods would be necessary to confirm presence of Helicobacter pylori as potential underlying pathogenetic mechanism of nasal polyposis.
Adult↗
Concentration of s-ICAM-1 in nasal polyps tissue.
INTRODUCTION: Polyps are a nasal condition considered to be inflammatory in nature. Pathophysiology of that disorder is not fully known. The role of ICAM-1 in inflammatory and immune response through its involvement in leukocyte adhesion dependent phenomena is proved to be important. The aim of the study was to establish the role of sICAM-1 in the inflammatory process in nasal polyps. MATERIAL AND METHODS: 27 patients (23 males and 4 females) with nasal polyposis and 12 (7 males and 5 females) controls with septal deviation were included in the study. All patients underwent routine surgical treatment (polypectomy, septoplasty). The collected tissues of polyps and nasal mucosa were homogenized, placed in 0.04M EDTA and centrifuged. sICAM-1 concentration in supernatant of polyps and nasal mucosa tissue were determined with the ELISA method (Genzyme, UK). RESULTS: In the polyps tissue we found a significantly higher concentration of sICAM-1 compared to the nasal mucosa of healthy subjects (6.74 +/- 5.31 ng/ml vs 0.28 +/- 0.13 ng/ml; p < 0.001). The elevated concentration of sICAM-1 was positively correlated with total tissue eosinophil count (r = 0.51; p < 0.01) and the duration of the disease (r = 0.628; p < 0.001). No correlation was found between sICAM concentration and the age of the patients subjected to examination. CONCLUSIONS: The increased level of sICAM-1 in polyps tissue indicates the role of the molecule in the development of chronic inflammation and probably in the patophysiology of nasal polyps.
Adult↗
Pathogenesis of nasal polyps: an update.
The cause of nasal polyp formation is still unknown. Genetic predisposition has been suggested, but there are scanty data to support such theories. Activated epithelial cells may be the major source of mediators inducing influx of inflammatory cells (mostly eosinophils) and proliferation and activation of fibroblasts leading to nasal polyp formation. Infectious agents (including viruses, bacteria, or fungi) may be potential primary factors activating nasal epithelial cells. Proinflammatory cytokines and growth factors play important roles in the persistence of mucosal inflammation associated with nasal polyps. Arachidonic acid metabolites seem to be particularly important in the pathogenesis of nasal polyps in patients with aspirin hypersensitivity rhinosinusitis/asthma syndrome.
Aspirin↗
Expression, localization, and significance of vascular permeability/vascular endothelial growth factor in nasal polyps.
BACKGROUND: The exact etiologic mechanisms leading to the formation of nasal polyps have remained largely obscure. A key phenomenon of this specific type of chronic inflammatory disease in nasal respiratory mucosa is remarkable edema. Vascular permeability/vascular endothelial growth factor (VPF/VEGF) plays an important role in inducing angiogenesis and modulating capillary permeability. OBJECTIVE: To study the expression and localization of VPF/ VEGF as a putative key factor in nasal polyp development. METHODS: Specimens of nasal polyps (n = 12) were harvested during endonasal sinus surgery in patients with polypous chronic rhinosinusitis. Specimens of healthy nasal respiratory mucosa (n = 12) served as controls and were obtained from inferior turbinates of patients undergoing surgery for nasal obstruction without signs and symptoms of inflammatory disease. Frozen sections were immunohistochemically stained for VPF/VEGF and quantitatively analyzed, using computer-based image analysis. RESULTS: The expression of VPF/VEGF in specimens of nasal polyps was significantly stronger than in specimens of healthy nasal mucosa of controls. VPF/VEGF in polypous tissue was mainly localized in vascular endothelial cells, in basal membranes and perivascular spaces, and in epithelial cells. CONCLUSION: The markedly increased expression in nasal polyps as opposed to healthy nasal mucosa suggests that VPF/VEGF may play a significant role in both the formation of nasal polyps and in the induction of heavy tissue edema. This finding is discussed with respect to the differential expression of cyclooxygenase (COX) isoenzymes-1 and -2 (COX-1 and COX-2) in nasal polyps was significantly stronger than in specimens of healthy nasal mucosa of controls. VPF/VEGF in polypous tissue was mainly localized in vascular endothelial cells, in basal membranes and perivascular spaces, and in epithelial cells. Conclusion: The markedly increased expression in nasal polyps as opposed to healthy nasal mucosa suggests that VPF/VEGF may play a significant role in both the formation of nasal polyps and in the induction of heavy tissue edema. This finding is discussed with respect to the differential expression of cyclooxygenase (COX) isoenzymes-1 and -2 (COX-1 and COX-2) in nasal polyps.
Adult↗
Mast cell ultrastructure in the inferior turbinate and stroma of nasal polyps.
Fourteen unselected adult patients with nasal polyps had ultrastructural examination of mast cells from matching biopsies of the polyp and inferior turbinate. Between three and 10 blocks were examined for each patient in both tissues and every mast cell that had a nucleus was photographed for study. Fifty-three mast cells were found within the stroma of nasal polyps and 54 in the submucosa of the inferior turbinate biopsies. The number of granules ranged between 13 and 167 (mean 60) for polyps and 18 and 148 (mean 61) in the inferior turbinate. The mast cells appeared essentially normal in the inferior turbinate of four patients. The degree of degranulation of the mast cells was calculated as in previous studies and then averaged for both the polyp and the inferior turbinate of each patient. There was greater degranulation in the nasal polyp compared to inferior turbinate (p = 0.03). These results were compared with mast cell degranulation found in the normal nose and in the inferior turbinate of patients with perennial allergic rhinitis which we previously published. The inferior turbinates in these patients were more degranulated than the normal nose (p = 0.0001) but were similar to that found in patients with perennial allergic rhinitis. This suggested that some degree of degranulation may occur throughout the nose in two thirds of the patients with nasal polyps which supports the theory that mast cell reactions are not limited to the polyps in a proportion of patients.
Adult↗
[The recurrent nasal polyp analysed by mRNA difference to demonstrate].
OBJECTIVE: To look for the correlated gene of nasal polyp. METHOD: The nasal polyp was analysed by mRNA difference to demonstrate, and the fragment of writing was analysed and appraised. RESULT: The amplification products of normal conchae tissue were compared with the nasal polyp tissue under the condition of background with one accord. The total 11 difference fragments were discovered during the 150-700 bp. One of the fragments (X-1) was completely homology with the section series of the eight chromosome long arm. There was a zine finger protein in the upper stream and the down stream. The fragment expressed in nasal polyp tissue. CONCLUSION: Based on polymerase chain reaction (pcr), using differential display R. T. PCR (DD-RTPCR) technique, the difference express gene of nasal polyp could be effectively compared with normal nasal conchae tissue or cells, the correlated gene of nasal polyp tissue could screened out. The fragment (X-1) that was completely homology with the section series of the eight chromosome long arm may be a new identified gene which cause the nasal polyp.
Adult↗
[Expression of the inducible isoform of nitric oxide synthase mRNA and the role in nasal polyps].
OBJECTIVE: To explore the pathogenesis of nasal polyps. The aim of this study is to detect the expression of inducible isoform of nitric oxide synthase (iNOS) in nasal polyp tissue, and to compare these findings with that in normal nasal turbinate. METHODS: We examined the expression of iNOS in human nasal polyps from patients undergoing nasal polypectomy (n = 8) and nasal turbinectomy(n = 6). The iNOS mRNA expression was determined by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The iNOS mRNA expression was significantly stronger in the nasal polyps (NP) than that in turbinate tissues (P < 0.01). CONCLUSIONS: iNOS expression is upregulated in NP, which indicate that iNOS and NO may play a potential role in the formation and growth of NP.
Adult↗
Mucin gene expression in nasal polyps.
CONCLUSIONS: A large set of mucin genes is expressed in nasal polyps. The expression pattern is complex and may reflect the wide spectrum of variables involved in polyp formation and progression. Prospective studies including subgroups of nasal polyps and involving substantial numbers of cases in each subgroup will be required to elucidate these variables and to understand how they affect mucus secretion. OBJECTIVE: At present, 15 of the 19 known mucin genes are expressed in the human airways. Nasal polyps might be expected to have a mucin expression pattern comparable to that of the airways. The aim of this study was to investigate mucin expression in nasal polyps. MATERIAL AND METHODS: Nasal polyp samples were obtained from 20 patients during functional endoscopic sinus surgery. Normal (control) sphenoid sinus mucosa was obtained from patients undergoing trans-sphenoid hypophysectomy. The expression of eight mucin genes (MUC1-4, -5AC, -5B, -6 and -7) was studied by in situ hybridization utilizing digoxigenin-labelled oligonucleotide probes. RESULTS: MUC6 and -7 were not expressed in sphenoid sinus mucosa, while all the studied mucin genes were expressed in nasal polyps. Expression patterns varied widely between individual polyps. The predominant epithelial mucin genes were MUC4, -5AC and -3, while MUC5B and -7 were mainly of glandular origin. MUC1, -2 and -6 were weakly expressed. The major alteration in gene expression in nasal polyps was found in the submucosal glands. MUC4 and -5AC represent a major component of both submucosal glands and epithelial cells in nasal polyps.
Biomarkers, Tumor↗