The role of COX-2, ALOX12 and iNOS genes in nasal polyposis

Conclusion: These data suggest that nitric oxide (NO), a gene product of iNOS, may play a physiological role in the upper airways and also NO is associated with inflammatory processes in the airways.

📌 3 Key Takeaways

🎯

Objective & Hypothesis:Objectives: The aim of this study was to investigate whether cyclooxygenase-2 (COX-2), arachidonate 12-lipoxygenase (ALOX12) and inducible nitric oxide synthase (iNOS) which are well-known mediators in inflammatory process play a role in nasal polyposis (NP) and to show their roles in initiation and progression of inflammation.

📊

Key Findings & Data:Patients and Methods: We investigated the expression levels of COX-2, ALOX12 and iNOS genes by Real-time polymerase chain reaction (PCR) method in NP and healthy nasal mucosa tissues obtained from 10 patients (4 females, 6 males; mean age 40.2 years; range 21 to 54 years).

💡

Conclusion & Impact:Conclusion: These data suggest that nitric oxide (NO), a gene product of iNOS, may play a physiological role in the upper airways and also NO is associated with inflammatory processes in the airways.

🔬Design:Research Article

📍Scope:Comprehensive Sample

⚙️Variables:Polimeraz zincir reaksiyonu · Nazal polipler · Nitrik oksit

Abstract

Objectives: The aim of this study was to investigate whether cyclooxygenase-2 (COX-2), arachidonate 12-lipoxygenase (ALOX12) and inducible nitric oxide synthase (iNOS) which are well-known mediators in inflammatory process play a role in nasal polyposis (NP) and to show their roles in initiation and progression of inflammation. Patients and Methods: We investigated the expression levels of COX-2, ALOX12 and iNOS genes by Real-time polymerase chain reaction (PCR) method in NP and healthy nasal mucosa tissues obtained from 10 patients (4 females, 6 males; mean age 40.2 years; range 21 to 54 years). Results: The mRNA levels of COX-2 expression observed in NP was found to be relatively increased, compared to the control tissue (p>0.05). The ALOX12 levels were relatively decreased (p>0.05), while the expression level of iNOS mRNA was significantly higher in NP tissue (p<0.05). Conclusion: These data suggest that nitric oxide (NO), a gene product of iNOS, may play a physiological role in the upper airways and also NO is associated with inflammatory processes in the airways.

Özet

Amaç: Çalışmamızda çeşitli enflamatuvar hastalıklarda etkileri bilinen siklooksijenaz-2 (COX-2), araşidonat 12-lipoksijenaz (ALOX12) ve indüklenebilir nitrik oksit sentaz (iNOS) genlerinin nazal polip (NP) olgusunda etkisinin olup olmadığı araştırıldı ve enflamasyonun oluşumuna ya da sürdürülmesine nasıl bir katkıda bulundukları gösterildi. Hastalar ve Yöntemler: On hastadan (4 kadın, 6 erkek; ort. yaş 40.2 yıl; dağılım 21-54 yıl) elde edilen NP ve sağlıklı nazal mukoza dokularında, gerçek zamanlı polimeraz zincir reaksiyonu (Real-time PCR) yöntemi ile COX-2, ALOX12 ve iNOS genlerinin mRNA ifadelenme düzeyleri araştırıldı. Bulgular: Nazal poliplerde gözlenen COX-2 ifadelenmesinin mRNA düzeyinin kontrol dokusuna göre kısmen artmış olduğu saptandı (p>0.05). ALOX12 ifadelenmesinin NP’lerde kısmen düştüğü (p>0.05), iNOS mRNA ifadelenme düzeyinin ise istatistiksel açıdan önemli ölçüde arttığı bulundu (p<0.05). Sonuç: Bu veriler, üst solunum yollarında iNOS gen ürünü nitrik oksitin (NO) yalnızca fizyolojik rol oynamadığı, ayrıca NP’de enflamatuvar süreçler ile de ilişkili olduğunu akla getirmektedir.

Keywords

Polimeraz zincir reaksiyonu Nazal polipler Nitrik oksit Siklooksijenaz 2 Polymerase Chain Reaction Nasal Polyps Nitric Oxide Cyclooxygenase 2

🔖

Cite This Article

ERGİN, V., YILMAZ, A., ÇELENK, F., USLU, S., İLERİ, F., MENEVŞE, A. (2012). The role of COX-2, ALOX12 and iNOS genes in nasal polyposis. Kulak Burun Boğaz İhtisas Dergisi, Cilt: 22 - Sayı: 5, 254–258. https://ajindex.com/articles/343069

📄 Full Text PDF Viewer

Open in New Tab ↗

↗New Tab

📄

PDF görüntüleyici hazırlanıyor...

References (13)

Kitapçı F, Muluk NB, Atasoy P, Koç C. Nazal polipler. Van Tıp Dergisi 2005;12:212-22
Stammberger H. Rhinoscopic surgery. In: Settipane GA, Lund VJ, Bernstein JM, Tos M, editors. Nasal polyps: Epidemiology, pathogenesis and treatment
Rhode Island: Oceanside Pub; 1997. p. 170
Pfaffl MW, Horgan GW, Dempfle L. Relative expression software tool (REST) for group-wise comparison and statistical analysis of relative expression results in real-time PCR. Nucleic Acids Res 2002;30:e36
Jedrzejczak-Czechowicz M, Lewandowska-Polak A, Bienkiewicz B, Kowalski ML. Involvement of 15-lipoxygenase and prostaglandin EP receptors in aspirin-triggered 15-hydroxyeicosatetraenoic acid generation in aspirin-sensitive asthmatics. Clin Exp Allergy 2008;38:1108-16
Yoshimura T, Yoshikawa M, Otori N, Haruna S, Moriyama H. Correlation between the prostaglandin D(2)/E(2) ratio in nasal polyps and the recalcitrant pathophysiology of chronic rhinosinusitis associated with bronchial asthma. Allergol Int 2008;57:429-36
Higashi N, Mita H, Ono E, Fukutomi Y, Yamaguchi H, Kajiwara K, et al. Profile of eicosanoid generation in aspirin-intolerant asthma and anaphylaxis assessed by new biomarkers. J Allergy Clin Immunol 2010;125:1084-1091
Mastalerz L, Sanak M, Gawlewicz-Mroczka A, Gielicz A, Cmiel A, Szczeklik A Thorax. Prostaglandin E2 systemic production in patients with asthma with and without aspirin hypersensitivity. Thorax 2008;63:27-34
Szczeklik A, Sladek K, Dworski R, Nizankowska E, Soja J, Shelter J, et al. Bronchial aspirin challenge causes specific eicosanoid response in aspirin-sensitive asthmatics. Am ] Respir Crit Care Med 1996;154:1608-14
Adamusiak AM, Stasikowska-Kanicka O, Lewandowska-Polak A; Danilewicz M, Wagrowska-Danilewicz M, Jankowski A, et al. Expression of arachidonate metabolism enzymes and receptors in nasal polyps of aspirin-hypersensitive asthmatics. Int Arch Allergy Immunol 2012;157:354-62
Schmid M, GödeU,Schâfer D, Wigand ME. Arachidonic acid metabolism in nasal tissue and peripheral blood cells in aspirin intolerant asthmatics. Acta Otolaryngol 1999;119:277-80
Roca-Ferrer J, Garcia-Garcia FJ, Pereda J, Perez-Gonzalez M, Pujols L, Alobid I, et al. Reduced expression of COXs and production of prostaglandin E(2) in patients with nasal polyps with or without aspirin-intolerant asthma. J Allergv Clin Immunol 2011;128:66-72
P_____§rez-Novo CA, Watelet JB, Claeys C, Van CauwenbergeP, BachertC. Prostaglandin, leukotriene,