Background: The anti-inflammatory effect of montelukast, a leukotriene receptor antagonist, in patients with bronchial asthma is not entirely clear. Basophils can release a variety of mediators, including histamine and leukotriens, which most likely play an active role in the late allergic response.
Objectives: To study the effect of montelukast (10 mg/day) on histamine and cysteinyl leukotriene release from basophils taken from 12 mild atopic asthmatic patients who took the drug for 4 weeks.
Methods: Basophils were withdrawn at baseline, and after 48 hours, 1 week, and 4 weeks of therapy. Histamine was measured by a radioenzymatic method and leukotrienes by immunologic assay. Histamine and cysLT release was measured spontaneously and following stimulation with interleukin-3 and anti-immunoglobulin E. Spirometry and symptom score were measured before and during treatment.
Results: During the treatment with montelukast there were no significant changes in spontaneous, IL-3 and anti-IgE-induced histamine release. cysLT release decreased significantly only after 4 weeks of treatment (from 2899 +/- 550 pg/ml at baseline to 2225 +/- 430 pg/ml at 4 weeks, P= 0.02).
Conclusions: Montelukast does not seem to affect the release of histamine from basophils but mildly inhibits the cysLT release seen after 4 weeks of treatment.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Biosynthetic pathway for leukotrienes is stimulated by lipopolysaccharide and cytokines in pig endometrial stromal cells.
Sci Rep
January 2025
Division of Reproductive Biology, Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Tuwima 10, Olsztyn, 10-748, Poland.
An inflammatory response is related to different inflammatory mediators generated by immune and endometrial cells. The links between lipopolysaccharide (LPS), cytokines, and leukotrienes (LTs) in endometrial stromal cells remain unclear. This study aimed to examine the influence of LPS, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-4 and IL-10 on 5-lipooxygenase (5-LO), LTA4 hydrolase (LTAH) and LTC4 synthase (LTCS) mRNA and protein abundances, and LTB4 and cysteinyl (cys)-LTs release including LTC4, by the cultured pig endometrial stromal cells, as well as on cell viability.
View Article and Find Full Text PDFA critical role for Macrophage-derived Cysteinyl-Leukotrienes in HIV-1 induced neuronal injury.
Brain Behav Immun
May 2024
University of California Riverside, School of Medicine, Division of Biomedical Sciences, 900 University Ave, Riverside, CA 92521, USA; Sanford Burnham Prebys Medical Discovery Institute, Infectious and Inflammatory Disease Center, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address:
Macrophages (MΦ) infected with human immunodeficiency virus (HIV)-1 or activated by its envelope protein gp120 exert neurotoxicity. We found previously that signaling via p38 mitogen-activated protein kinase (p38 MAPK) is essential to the neurotoxicity of HIVgp120-stimulated MΦ. However, the associated downstream pathways remained elusive.
View Article and Find Full Text PDFMonoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
Front Allergy
April 2023
Department of Microbiology, Immunology and Transplantation, KULeuven, Leuven, Belgium.
Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. N-ERD results in associated asthma exacerbations, oral corticosteroids bursts, corticosteroid-dependent disease, and multiple endoscopic sinus surgeries.
View Article and Find Full Text PDFWhat happens to basophils and tryptase, LXA and CysLTs during aspirin desensitization?
J Asthma
August 2023
Department of Chest Disease, Division of Immunology and Allergy, Ankara University School of Medicine, Dikimevi/Ankara, Turkey.
Introduction: Aspirin desensitization (AD) is an effective treatment in patients with non-steroidal anti-inflammatory drugs (NSAID)-exacerbated respiratory disease (NERD) by providing inhibitory effect on symptoms and polyp recurrence. However, limited data is available on how AD works. We aimed to study comprehensively the mechanisms underlying AD by examining basophil activation (CD203c upregulation), mediator-releases of tryptase, CysLT, and LXA, and LTB receptor expression for the first 3 months of AD.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!