2003
DOI: 10.1067/mai.2003.1491
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Abstract: Our results point to a deficient PGE(2) production under proinflammatory conditions in asthmatic airways. This could weaken local defensive mechanisms and promote cysteinyl leukotriene overproduction.

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Cited by 124 publications
(154 citation statements)
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“…Similarly, other studies have also shown a significantly low production of PGE 2 in cultured bronchial fibroblasts from AIA [13].…”
Section: Discussionmentioning
confidence: 95%
See 1 more Smart Citation
“…Similarly, other studies have also shown a significantly low production of PGE 2 in cultured bronchial fibroblasts from AIA [13].…”
Section: Discussionmentioning
confidence: 95%
“…In patients with asthma, and especially in AIA, various data support the existence of an altered regulation of the COX pathway [9][10][11][12][13][14][15]. PGE 2 levels have been reported to be low in the nasal polyps of asthma patients, as well as in nasal-polyp and bronchial fibroblasts from asthmatic patients, particularly those with aspirin sensitivity [11,[13][14][15]. As PGE 2 production mostly depends on the level of COX-2 induction under conditions of inflammation, it should be expected that the low production of PGE 2 detected in asthma and nasal polyps would be accompanied by a similar, concomitant alteration in the expression of COX-2.…”
Section: Introductionmentioning
confidence: 99%
“…Although the underlying mechanisms of AIA have not been elucidated completely, arachidonic acid metabolites such as prostaglandins (PGs), leukotrienes (LTs), and thromboxane (TBX) are reportedly involved in the pathogenesis of this asthma phenotype (8)(9)(10). Anti-inflammatory PGs are one of the various types of oxygenated metabolites generated by the cyclooxygenase (COX) pathway that function to reduce the level of PGE2, the main COX2 metabolite (11)(12)(13). The cyclooxygenase theory is widely accepted as responsible for the pathogenesis of AIA.…”
Section: Introductionmentioning
confidence: 99%
“…2,4 Overproduction of CysLTs and deficiency of prostaglandin E 2 in bronchial fibroblasts by COX inhibition have been proposed to have crucial roles in AERD development. 4,15 However, along with conflicting results for the associations between polymorphisms of genes in leukotriene and COX pathways [16][17][18] genes on other pathways including bronchial hyperresponsiveness by MHC or structural genes have provided new insights for AERD pathogenesis. 5,19 Therefore, although further replications and functional evaluations are required, our findings on the associations of TAP2 with AERD-related symptoms, particularly with FEV1 decline by aspirin provocation, might provide evidences for the role of the gene in respiratory deficiencies.…”
Section: Discussionmentioning
confidence: 99%