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Nasal Polyp Tissue (nasal + polyp_tissue)
Selected AbstractsApoptosis and Phagocytosis of Tissue-Dwelling Eosinophils in Sinonasal Polyps,THE LARYNGOSCOPE, Issue 1 2000Ĺke Davidsson MD Abstract Objective: Sinonasal polyps contain numerous tissue-dwelling eosinophils, but the mechanisms causing their accumulation, functional activities, and resolution are largely unknown. Study Design: Nasal polyp tissue from 14 patients was evaluated for cellular expression of CD95, CD68, and Annexin-V, for the degree of apoptosis, and for phagocytosis of eosinophils. Material and Methods: Histological sections were immunostained as single stains for CD95, CD68, and Annexin-V, and as an immunostaining for CD68 combined with a modified Vital New Red staining. The latter staining is specific for eosinophils. Other sections were stained by terminal d-UTP nick end labeling (TUNEL) assay and routinely stained for H&E. Evaluation of the amount of stained cells was performed by counting the average number in 10 randomly chosen high-power fields. The TUNEL positivity was in all cases confirmed with apoptotic morphology. Results: The inflammatory infiltrate consisted of numerous eosinophils but also a considerable amount of lymphocytes, mast cells, and macrophage-like CD68+ cells. CD95 was frequently expressed on eosinophils, on numerous other inflammatory cells, and also on morphologically apoptotic cells. Annexin-V-positive eosinophils were not as frequent as CD95+ cells, but numerous Annexin-V-positive eosinophils were found. CD68+ cells approximately equalled the number of eosinophils. The number of cells phagocytosing eosinophils varied between polyps. Apoptosis of eosinophils (as evaluated by TUNEL combined with apoptotic morphology) was a common finding in six of the polyps. Conclusions: Previous in vitro and ex vivo findings of CD95 on eosinophils are now supported by demonstration of CD95 on eosinophils in this in vivo study. This investigation revealed a switch of the membrane-bound phosphatidylserine of apoptotic cells, which is a novel observation. The study has demonstrated apoptosis of tissue-dwelling eosinophils, and that CD68+ macrophage-like cells phagocytose eosinophils within the sinonasal polyps. [source] CRTH2 mediates the activation of human Th2 cells in response to PGD2 released from IgE/anti-IgE treated nasal polyp tissueALLERGY, Issue 3 2010C. A. Pérez-Novo To cite this article: Pérez- Novo CA, Holtappels G, Vinall SL, Xue L, Zhang N, Bachert C, Pettipher R. CRTH2 mediates the activation of human Th2 cells in response to PGD2 released from IgE/anti-IgE treated nasal polyp tissue. Allergy 2010; 65: 304,310. Abstract Background:, Mast cells release mediators upon stimulation that contribute to the pathogenesis of chronic airway disease, including the recruitment and activation of Th2 lymphocytes. The objective was to determine the involvement of prostaglandin D2 (PGD2) and its receptors in the chemotaxis of Th2 cells, using nasal polyp tissue. Methods:, Tissue explants from ten patients with nasal polyposis were incubated with RPMI alone or RPMI containing IgE/anti-IgE for 30 min. Some samples were treated with diclofenac to inhibit the production of PGD2. Supernatants were assayed for PGD2 content and for their ability to promote human Th2 cell chemotaxis in the presence and absence of a CRTH2 antagonist. Transcript levels of D protanoid receptor type 1 (DP1), chemoattractant receptor-homologous receptor expressed on Th2 cells (CRTH2) and PGD2 synthase were analysed by real time PCR. Results:, Increased release of PGD2 by nasal polyp tissue treated with IgE/anti-IgE was significantly inhibited by preincubation of the tissue with diclofenac. Transcript levels of PGD2 synthase, DP1 and CRTH2 receptors increased after stimulation with IgE/anti-IgE. Supernatants from IgE/anti-IgE-stimulated nasal polyp tissue caused significantly increased chemotaxis of Th2 cells. The levels of PGD2 produced and the degree of Th2 cell chemotaxis were highly correlated. Diclofenac inhibited the production of Th2 cell chemotactic activity, and the chemotactic effect of the supernatant on Th2 cells was inhibited by the CRTH2 antagonist ramatroban. Conclusion:, These data suggest that in immunologically activated nasal polyp tissue, PGD2 produced by mast cells promotes the migration of Th2 cells through a CRTH2 dependent mechanism. [source] Gene Expression Profiling of Nasal Polyps Associated With Chronic Sinusitis and Aspirin-Sensitive Asthma,THE LARYNGOSCOPE, Issue 5 2008Konstantina M. Stankovic MD Abstract Objective: To identify genes whose expression is most characteristic of chronic rhinosinusitis and aspirin-sensitive asthma through genome-wide transcriptional profiling of nasal polyp tissue. Study Design: Prospective, controlled study conducted at a tertiary care institution. Methods: Thirty genome-wide expression microarrays were used to compare nasal polyp tissue from patients with chronic rhinosinusitis alone (CRS, n = 10) or chronic rhinosinusitis and a history of aspirin-sensitive asthma (ASA, n = 10) to normal sinonasal mucosa from patients who underwent surgery for non-sinus related conditions (controls, n = 10). Genes found to be most characteristic of each polyp phenotype, as determined from bioinformatic analyses, were validated using real-time quantitative polymerase chain reaction (RT-PCR) and immunohistochemistry in different patient sets. Results: The transcriptional signature of the control mucosa was distinctly different from that of either polyp phenotype. Genes most characteristic of the CRS phenotype included two upregulated genes,met proto-oncogene (MET) and protein phosphatase 1 regulatory subunit 9B (PPP1R9B),and two downregulated genes, prolactin-induced protein (PIP) and zinc alpha2-glycoprotein (AZGP1). The gene most characteristic of the ASA phenotype was periostin (POSTN), which was upregulated relative to controls. Differences between the CRS and ASA phenotypes were associated with alterations in the 6p22, 22q13, and 1q23 chromosomal regions. Conclusions: Nasal polyps appear to have characteristic transcriptional signatures compared to normal sinonasal mucosa. The five genes identified in this study likely play roles in the pathogenesis of polyps associated with CRS and ASA, and are therefore attractive targets for novel medical therapies for these common debilitating diseases. [source] Prevalence of Helicobacter pylori in Patients with Nasal Polyps: A Preliminary ReportTHE LARYNGOSCOPE, Issue 11 2004Can Koc MD Abstract Objectives: The aim of the study is to determine the presence of H. pylori in nasal polyps by both immunohistochemical staining with H. pylori antibody of biopsy specimens and enzyme-linked immunoadsorbent assay (ELISA) of sera. Study Design: A prospective, controlled, clinical trial. Methods: We enrolled 30 patients with nasal polyps and 20 controls with middle concha bullosa undergoing endoscopic sinus surgery (ESS). Blood samples of both the study and control groups were evaluated for anti- H. pylori specific immunoglobulin (Ig)G antibodies by ELISA. In addition, biopsy specimens of the removed polyps and the mucosal part of middle conchas were examined by the immunohistochemical analysis with H. pylori antibody. Results: In the blood samples, specific IgG antibodies to H. pylori were found in 26 (86.7%) of 30 polyp patients and 17 (85%) of 20 controls. In 6 (20%) of the 30 patients, H. pylori was identified in the nasal polyp tissue, but it was not detected in the mucosal part of the middle concha specimens. No significant statistical difference was observed for H. pylori antibodies by ELISA among the patients with nasal polyps and the control group (Fisher's exact test, P = .59). However, there was a statistical difference between the polyp biopsy specimens and the control biopsy specimens by immunohistochemical staining (Fisher's exact test, P = .037). Conclusions: This study indicates that H. pylori was found in increased prevalence in the nasal polyps. However, further controlled epidemiologic studies would be necessary to confirm our results and clarify the potential underlying pathogenetic mechanisms. [source] | ||||||||||