Effect of Nedocromil Sodium on Sulfidopeptide Leukotrienes-stimulated Human Alveolar Macrophages in Asthma

✍ Scribed by T. Radeau; Ph. Godard; C. Chavis; F.B. Michel; B. Descomps; M. Damon

• Publisher: Elsevier
• Year: 1993
• Tongue: English
• Weight: 263 KB
• Volume: 6
• Category: Article
• ISSN: 0952-0600
• DOI: 10.1006/pulp.1993.1005

✦ Synopsis

SUMMARY: Alveolar macrophages (AM) may take part in the amplification of the inflammatory mechanism involved in asthma. During an asthma attack, mast cells and eosinophils release arachidonic acid derivative mediators of inflammation such as sulfidopeptide leukotrienes. Among them, (\mathrm{LTC}{4}) has been shown to be present in bronchoalveolar fluid. In asthmatic patients, we showed that the ability of AM to transform (\mathrm{LTC}{4}) into its derivatives LTD ({4}) and LTE ({4}) was related to the intensity of the local inflammation observed during endoscopy. AM from asthmatics incubated in the presence of (\mathrm{LTC}{4}) or (\mathrm{LTE}{4}), generated (\mathrm{LTB}{4}) and (5-\mathrm{HETE}), which are potent chemoattractants. Nedocromil sodium (\left(10^{-4} \mathrm{M}\right)) decreased (\mathrm{LTB}{4}) releasability and intracellular 5-HETE concentrations in zymosan-stimulated AM from asthmatic patients, and was shown to decrease the LTC ({4}) or LTE ({4})-promoted formation of (\mathrm{LTB}_{4}) and 5-HETE.