Eicosanoid mediator expression in mononuclear and polymorphonuclear cells in normal subjects and patients with atopic asthma and cystic fibrosis
| Autor: | L. M. Kuitert, P. J. Barnes, Robert Newton, Neil Barnes, Ian M. Adcock |
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| Předmět: |
Adult
Male Pulmonary and Respiratory Medicine medicine.medical_specialty Allergy Pancreatic disease Cystic Fibrosis Transcription Genetic Neutrophils 5-Lipoxygenase-Activating Proteins Polymerase Chain Reaction Cystic fibrosis Internal medicine medicine Arachidonate 15-Lipoxygenase Humans 5-lipoxygenase-activating protein Asthma Leukotriene Arachidonate 5-Lipoxygenase biology business.industry Membrane Proteins Middle Aged medicine.disease Isoenzymes Endocrinology Eicosanoid Prostaglandin-Endoperoxide Synthases Arachidonate 5-lipoxygenase Immunology Leukocytes Mononuclear biology.protein Eicosanoids Female Carrier Proteins business Research Article |
| Zdroj: | Scopus-Elsevier |
| Popis: | BACKGROUND: Eicosanoids such as leukotrienes, prostaglandins, lipoxins, and 15-hydroperoxyeicosatetraenoic acid (15-HETE) cause bronchoconstriction, increased microvascular permeability, mucus secretion, and polymorph chemotaxis. These pro-inflammatory effects are important in diseases such as asthma and cystic fibrosis where the levels of mediators are increased both in the stable and acute state. A study was conducted to examine the expression of the mRNA for the enzymes of the eicosanoid pathways (5-lipoxygenase (5-LO), 5-lipoxygenase activating protein (FLAP), cyclo-oxygenases 1 and 2 (COX-1, COX-2), and 15-lipoxygenase (15-LO)) in normal subjects and in patients with stable atopic asthma and stable cystic fibrosis. METHODS: Reverse transcription polymerase chain reaction (RT-PCR) was used to examine the expression of total RNA for 5-LO, FLAP, COX-1, COX-2, and 15-LO in peripheral blood polymorphonuclear cells and mononuclear cells from the three subjects groups. RESULTS: The expression of mRNA for 5-LO and FLAP was similar in normal subjects and in patients with asthma and cystic fibrosis. COX-1 was increased in both cell types in asthmatic patients. COX-2 and 15-LO were increased in polymorphs of patients with atopic asthma but not in mononuclear cells. COX-2 and 15-LO were undetectable in either cell type in patients with cystic fibrosis whereas COX-1 levels in polymorphs were similar to those in patients with asthma. CONCLUSIONS: The increased leukotriene production in asthma and cystic fibrosis is not explained by an increase in transcription of 5-LO and FLAP. Transcription of 15-LO and COX-2 is increased in atopic asthma. Transcription of COX-1 is increased in both atopic asthma and cystic fibrosis. |
| Databáze: | OpenAIRE |
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