Cyclooxygenase and lipoxygenase metabolite generation in nasal polyps

Pinto, Stefania; Gallo, Oreste; Polli, G.; Boccuzzi, Simone; Paniccia, Rita; Brunelli, Tamara; Abbate, Rosanna

doi:10.1016/s0952-3278(97)90556-1

Cited by 33 publications

(30 citation statements)

References 16 publications

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“…In nasal polyps from allergic patients, significantly higher LTB 4 levels were observed along with a tendency to produce higher amounts of COX products in comparison with nonallergic subjects, whereas in turbinates of nonallergic patients LT levels were significantly higher in comparison to those with allergic rhinitis. Patients with aspirin-sensitive asthma had a decreased COX/LO ratio, supporting the hypothesis of an imbalance of AA metabolism in this syndrome [36].…”

Section: Role Of Cox and Pgs In Crs And Nasal Polypssupporting

confidence: 53%

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Cyclooxygenases and the pathogenesis of chronic rhinosinusitis and nasal polyposis

Guilemany¹,

Roca‐Ferrer²,

Mullol

2008

Curr Allergy Asthma Rep

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Cyclooxygenase (COX) enzymes catalyze the rate-limiting steps in prostaglandin synthesis. Prostaglandins have an important role in several physiological processes such as maintenance of gastrointestinal integrity and pathological processes such as inflammation and neoplasia. Several mechanisms have been proposed for the development of chronic rhinosinusitis, but the common final pathway seems to be an integrated process involving the mucosal epithelium, matrix, and inflammatory cells and mediators. Upper and lower airway pathologies coexist and share common etiopathogenic mechanisms, and nasal polyposis is often associated with asthma and aspirin sensitivity. The cellular source of COX activity in acute and chronic inflammation, as in chronic rhinosinusitis, is poorly understood. COX theory postulated that inhibition of COX broke down biochemical reactions that lead to the development of asthma attacks. This article focuses on COX in the pathogenesis of chronic rhinosinusitis and nasal polyposis.

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Section: Role Of Cox and Pgs In Crs And Nasal Polypssupporting

confidence: 53%

“…Previous studies showed elevated basal levels of peptido-leukotrienes and reduced basal levels of PGE 2 in aspirin-sensitive patients and quite the reverse in aspirintolerant patients [35][36][37][38][39].…”

Section: Role Of Cox and Pgs In Crs And Nasal Polypsmentioning

confidence: 99%

Cyclooxygenases and the pathogenesis of chronic rhinosinusitis and nasal polyposis

Guilemany¹,

Roca‐Ferrer²,

Mullol

2008

Curr Allergy Asthma Rep

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“…24 PGE 2 and COX-2 enzyme have been found to be decreased in peripheral blood cells and nasal polyp tissue from patients with aspirin sensitivity. 25 In addition, the cyclooxygenase/lipoxygenase ratio is downregulated in the nasal tissue from aspirin-sensitive patients compared with nonsensitive and control subjects, 26 suggesting that a deficit of this prostanoid might be responsible for the chronic inflammatory reactions in these diseases. The aim of this study was to analyze the local tissue eicosanoid production in 3 subgroups of patients with CRS and to evaluate the possible correlation with the severity of eosinophilic inflammation and the clinical manifestation of aspirin sensitivity.…”

mentioning

confidence: 99%

Prostaglandin, leukotriene, and lipoxin balance in chronic rhinosinusitis with and without nasal polyposis

Pérez-Novo

Watelet

Claeys

et al. 2005

Journal of Allergy and Clinical Immunology

263

247

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“…Most researchers agree with the production of several types of PGs during allergic reaction in human and experimental animals. [16][17][18][19][20] But each researcher has failed to obtain consensus in terms of the effect of the PG inhibitors on allergic response and the magnitude of allergic response caused by each PG. So, in this review, we focused on the experimental results employing PG synthesis inhibitor, indomethacin, and PG receptor gene manipulated mice on allergic reaction in mice.…”

Section: The Role Of Pgs In Allergic Inflam-mationmentioning

confidence: 99%

Prostaglandin as a Target Molecule for Pharmacotherapy of Allergic Inflammatory Diseases

Nagai

2008

Allergology International

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The purpose of this review is to summarize the role of prostaglandins (PGs) in allergic inflammation and to know the value of PGs, as a target molecule for an anti-allergic drug. PGD(2) is the major PG produced by the cyclooxygenase pathway in mast cells. Our and others findings indicate that PGD(2) is one of the potent allergic inflammatory mediators and must be a target molecule of anti-allergic agent. From our data, one of PGD(2) receptor antagonists show clear inhibition of airway hypersensitivity caused by allergic reaction. Concerning the role of PGE(2) in allergic inflammation, conflicting results have been reported. Many experimental data suggest an individual role of each PGE(2) receptor, EP(1), EP(2), EP(3) and EP(4) in allergic reaction. Our results indicate the protective action of PGE(2) on allergic reaction via EP(3). In addition, one of EP(3) agonists clearly inhibits the allergic airway inflammation. These findings indicate the value of EP(3) agonists as an anti-allergic agent. In addition, some investigators including us reported that PGI(2) plays an important role for the protection of the onset of allergic reaction. However, the efficacy of PGI(2) analogue as an anti-allergic agent is not yet fully investigated. Finally, the role of thromboxane A(2) (TxA(2)) in allergic reaction is discussed. Our experimental results suggest a different participation of TxA(2) in allergic reaction of airway and skin. In this review, the role of PGs in allergic inflammation is summarized and the value of PGs as a target molecule for developing a new anti-allergic agent will be discussed.

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Cyclooxygenase and lipoxygenase metabolite generation in nasal polyps

Cited by 33 publications

References 16 publications

Cyclooxygenases and the pathogenesis of chronic rhinosinusitis and nasal polyposis

Cyclooxygenases and the pathogenesis of chronic rhinosinusitis and nasal polyposis

Prostaglandin, leukotriene, and lipoxin balance in chronic rhinosinusitis with and without nasal polyposis

Prostaglandin as a Target Molecule for Pharmacotherapy of Allergic Inflammatory Diseases

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