Sulfite Induces Release of Lipid Mediators by Alveolar Macrophages

Author:

Beck-Speier Ingrid1,Dayal Niru1,Denzlingerb Claudio2,Haberl Christopher3,Maier Konrad L.1

Affiliation:

1. GSF - National Research Center for Environment and Health, Institute for Inhalation Biology, D-85764 Neuherberg/München, Germany

2. Department II, Medical Clinic, University of Tübingen, D-72076 Tübingen, Germany

3. Department III, Medical Clinic, University of Munich, D-81377 München, Germany

Abstract

Abstract Air pollutants are supposed to modulate physiological responses of alveolar macrophages (AM ). This study was addressed to the question whether at neutral pH sulfur(IV) species in comparison to sulfur(VI) species cause AM to release proinflammatory mediators and which pathways are involved in their generation. Supernatants obtained from canine AM treated with sulfite (0.1 mᴍ to 2 mᴍ) enhanced the respiratory burst of canine neutrophils, measured by lucigenin-dependent chemiluminescence, whereas supernatants derived from AM treated with sulfate (1 mᴍ) did not. The neutrophil-stimulating activity released by sulfite-treated AM consisted of platelet-activating factor (PAF) and leukotriene B4 (LTB4) as shown by desensitization of the corresponding receptors. Inhibitors of phospholipase A2 substantially suppressed release of neutrophil-stimulating activity by sulfite-treated AM. Inhibition of 5- lipoxygenase in sulfite-treated AM also reduced neutrophil-stimulating activity, while inhibition of cyclooxygenase had no effect. In conclusion, sulfite induces AM to release lipid mediators via phospholipase A2- and 5-lipoxygenase-dependent pathways. These mediators activate neutrophils via the receptors for PAF and LTB4.

Publisher

Walter de Gruyter GmbH

Subject

General Biochemistry, Genetics and Molecular Biology

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