Cellular Source of Cysteinyl Leukotrienes following Chlorine Exposure

American Journal of Respiratory Cell and Molecular Biology
Toby K McGovernJames G Martin

Abstract

Exposure of the mouse to high concentrations of chlorine leads to the synthesis of cysteinyl leukotrienes (cysLTs). CysLTs contribute to chlorine-induced airway hyperresponsiveness. The aim of the current study was to determine the cellular source of the cysLTs. To achieve this aim we exposed mice to 100 ppm of chlorine for 5 mins. Intranasal instillation of clodronate in liposomes and of diphtheria toxin in CD11c-DTR mice was used to deplete macrophages. CCR2-/- mice were used to assess the contribution of recruited macrophages. Eosinophils and neutrophils were depleted with specific antibodies. Platelet-neutrophil aggregation was prevented with an antibody against P-selectin. The potential roles of phagocytosis of neutrophils by macrophages and of transcellular metabolism between epithelial cells and neutrophils were explored in co-culture systems. We found that depletion of neutrophils was the only intervention that inhibited the synthesis of cysLTs at 24h after chlorine exposure. While macrophages did synthesize cysLTs in response to phagocytosis of neutrophils, depletion of macrophages did not reduce the increment in cysLTs triggered by chlorine exposure. However, co-culture of airway epithelial cells with neutrophils resu...Continue Reading

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Citations

Aug 29, 2020·American Journal of Respiratory Cell and Molecular Biology·Peter H S Sporn
Aug 18, 2021·Clinical Science·William S Powell
Jun 29, 2021·American Journal of Respiratory and Critical Care Medicine·Andrew J HalaykoPrescott G Woodruff

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Methods Mentioned

BETA
Flow Cytometry

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