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Pro-inflammatory response of alveolar macrophages induced by sulphite: studies with lucigenin-dependent
I Beck-Speier1, N Dayal, K L Maier
1GSF-National Research Centre for Environment and Health, Institute for Inhalation Biology, Neuherberg/Munich, Germany.
Abstract:
Alveolar macrophages (AM) were studied for their capability to release mediators involved in modulation of neutrophil (PMN) functions. Initial responses were induced by sulphite. Supernatants obtained from canine, human and rat AM pre-treated with sulphite in concentrations of 0.1-2 mmol/L enhanced the respiratory burst of canine, human and rat PMN, measured by lucigenin-dependent chemiluminescence (CL). This PMN-stimulating activity exhibited platelet-activating factor (PAF)-like properties, as indicated by desensitization of the PAF receptor, inhibition with PAF antagonists WEB 2086 and CV 3988, and the kinetic CL response like PAF after chloroform extraction of supernatants inhibitable by PAF antagonist CV 3988. These results indicate that AM are triggered by sulphite to release mediators that activate the respiratory burst of PMN, primarily via the PAF receptor.
Insights
Sulphite exposure triggers alveolar macrophages (AM) to release mediators that activate neutrophil (PMN) respiratory bursts, primarily through platelet-activating factor (PAF) receptors. This finding highlights a novel mechanism in inflammatory responses.
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Alveolar macrophages (AM) play a crucial role in lung immunity.
- Neutrophil (PMN) functions are critical in host defense and inflammation.
- The interaction between AM and PMN is key to inflammatory processes.
Purpose of the Study:
- To investigate the capacity of AM to release mediators that modulate PMN functions.
- To determine the effect of sulphite exposure on AM-mediated PMN activation.
- To elucidate the mechanism by which AM influence PMN respiratory burst.
Main Methods:
- Canine, human, and rat AM were pre-treated with sulphite.
- Supernatants from AM were applied to PMN.
- Neutrophil respiratory burst was measured using lucigenin-dependent chemiluminescence (CL).
- Platelet-activating factor (PAF) receptor involvement was assessed using receptor desensitization and PAF antagonists (WEB 2086, CV 3988).
Main Results:
- Sulphite-induced AM supernatants enhanced PMN respiratory burst in canine, human, and rat models.
- The observed PMN-stimulating activity demonstrated PAF-like properties.
- Inhibition by PAF antagonists and specific kinetic responses confirmed PAF receptor pathway involvement.
- Chloroform extraction and subsequent inhibition by CV 3988 further supported PAF mediation.
Conclusions:
- Alveolar macrophages are activated by sulphite to release mediators.
- These mediators, primarily acting via the PAF receptor, enhance neutrophil respiratory burst.
- This study reveals a sulphite-induced inflammatory pathway involving AM and PMN activation.