Biosynthesis of cysteinyl‐leucotrienes in aspirin‐intolerant asthma

Sanak, Marek; Sampson,

doi:10.1046/j.1365-2222.1999.00443.x

Cited by 43 publications

(29 citation statements)

References 42 publications

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“…In humans, it has been suggested that increased production of cysteinyl-LT correlates with susceptibility to aspirin-intolerant asthma (37,38). Recent studies have shown that variations in the synthesis of cysteinyl-LT result from a polymorphism in the LTC 4 synthase gene promoter, which causes constitutive overexpression of this enzyme in aspirin-sensitive patients (37)(38)(39)(40). Differing expression levels of LTC 4 synthase may account for variability observed in the response to LT inhibitors used in the treatment of asthma (37).…”

Section: Discussionmentioning

confidence: 99%

“…It is also possible that differences in the production of and/or response to LTB 4 may contribute to the strain variation seen in the 5LO-dependent component of inflammatory responses. In humans, it has been suggested that increased production of cysteinyl-LT correlates with susceptibility to aspirin-intolerant asthma (37,38). Recent studies have shown that variations in the synthesis of cysteinyl-LT result from a polymorphism in the LTC 4 synthase gene promoter, which causes constitutive overexpression of this enzyme in aspirin-sensitive patients (37)(38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

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Genetic Factors Determine the Contribution of Leukotrienes to Acute Inflammatory Responses

Goulet

Byrum

Key

et al. 2000

The Journal of Immunology

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Leukotrienes (LT) are potent lipid mediators synthesized by the 5-lipoxygenase pathway of arachidonic acid (AA) metabolism. LT have been implicated in a broad spectrum of inflammatory processes. To investigate the influence of genetic factors on the contribution of LT to acute inflammation, we generated congenic 5-lipoxygenase-deficient 129, C57BL/6 (B6), and DBA/1Lac (DBA) mouse lines. Topical application of AA evoked a vigorous inflammatory response in 129 and DBA mice, whereas only a modest response was seen in B6 animals. The response to AA in 129 and DBA strains is LT dependent. In contrast, LT make little contribution to this response in B6 mice. AA-induced inflammation in B6 mice is prostanoid dependent, since this response was substantially reduced by treating B6 mice with a cyclooxygenase inhibitor. These data suggest that prostanoids are essential for AA-induced cutaneous inflammation in B6 mice, whereas LT are the major mediators of this response in 129 and DBA strains. In contrast, the response to AA in the peritoneal cavity is robust in the 129 and B6 strains, but was significantly blunted in DBA mice, showing that strain differences in the response to AA are tissue specific. Variations in these and other experimental models of inflammation appear to correlate directly with the ability of a particular mouse strain and a specific tissue to respond to LT, specifically LTC4. Taken together, these findings indicate that the relative contribution of prostanoids and LT to inflammatory responses is variable not only between strains but also between different tissues within these inbred mouse lines.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Genetic Factors Determine the Contribution of Leukotrienes to Acute Inflammatory Responses

Goulet

Byrum

Key

et al. 2000

The Journal of Immunology

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“…Many patients with AIA have been noted to synthesize large amounts of leukotriene C 4 synthase (LTC 4 S) leading to excessive production of CysLTs, known potent mediators of inflammation in asthma. 22,23 In addition, genetic polymorphism of the LTC 4 S promoter has been linked to increased production of CysLTs in some patients with AIA. 24 Overexpression of CysLT receptors on cells involved in the inflammatory cascade of asthma may also predispose patients to NSAID-induced bronchospasm.…”

Section: Discussionmentioning

confidence: 99%

The Prevalence of Ibuprofen-sensitive Asthma in Children: A Randomized Controlled Bronchoprovocation Challenge Study

Debley

Carter

Gibson

et al. 2005

The Journal of Pediatrics

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“…Tatsächlich sind unsere Kenntnisse über das "intrinsic" Asthma spärlich. Lediglich Subgruppen von Patienten mit Aspirin-sensitivem Asthma (ASA) sind vergleichsweise gut charakterisiert [31,124,127,139] [57].…”

Section: Klinische Aspekteunclassified

Pathogenese des Asthma bronchiale – Eröffnung neuer therapeutischer Perspektiven

Beeh¹,

Buhl²

2001

Med Klin

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The recent insights from molecular biology have found their correlate in actual therapeutic guidelines, and have further led to the development of new innovative asthma drugs such as monoclonal antibodies against IgE or IL-5. Hopefully, future progress in revealing pathogenetic mechanisms of asthma may lead to further therapeutic improvement and eventually reverse the trend of rising asthma morbidity in western societies.

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Biosynthesis of cysteinyl‐leucotrienes in aspirin‐intolerant asthma

Cited by 43 publications

References 42 publications

Genetic Factors Determine the Contribution of Leukotrienes to Acute Inflammatory Responses

Genetic Factors Determine the Contribution of Leukotrienes to Acute Inflammatory Responses

The Prevalence of Ibuprofen-sensitive Asthma in Children: A Randomized Controlled Bronchoprovocation Challenge Study

Pathogenese des Asthma bronchiale – Eröffnung neuer therapeutischer Perspektiven

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