Interleukin-13, but Not Indomethacin, Increases Cysteinyl-Leukotriene Synthesis in Human Lung Macrophages. (29th October 2011)

• Record Type: Journal Article
• Authors: Jackson, Sarah E.; Holloway, John W.; Warner, Jane A.; Sampson, Anthony P.
• Other Names: Teran Luis M. Academic Editor.
• Is Part Of: Journal of allergy. Volume 2012(2012)
• Publication Date: 2011-10-29
• Subjects: Allergy -- Periodicals; Immunologic diseases -- Periodicals; Allergy and Immunology; Hypersensitivity; Immune System Diseases; Allergy; Immunologic diseases; Electronic journals; Periodical; Periodicals; 616.97
• DOI: 10.1155/2012/348741
• Languages: English
• ISSNs: 1687-9783

Abstract

Abstract : Aspirin-exacerbated respiratory disease (AERD) is associated with constitutively elevated synthesis of bronchoconstrictor cysteinyl-leukotrienes, associated with increased expression of leukotriene (LT)C4 synthase and Th2 cytokines and airway eosinophilia. We examined whether interleukin-13 can increase LTC4 synthase gene transcription and cysteinyl-leukotriene synthesis in macrophages isolated from resected human lung tissue and whether an NSAID (indomethacin) can trigger further cysteinyl-leukotriene synthesis in these cells. Overnight culture of human lung macrophages with IL-13 (10 ng/mL) increased spontaneous and ionophore-stimulated production of cysteinyl-leukotrienes by 42% (P = 0.02 ) and 52% (P = 0.005 ), respectively, as quantified by enzyme immunoassays, but PCR gene transcription assays did not demonstrate an effect on LTC4S mRNA. The addition of indomethacin (100 μM) did not modulate cysteinyl-leukotriene production in either IL-13-treated or untreated macrophages. We conclude that while IL-13 enhances cysteinyl-leukotriene synthesis in human lung macrophages, it does not replicate the enhanced LTC4 synthase expression observed in the AERD lung nor confer sensitivity to NSAIDs.