Ozone-derived oxysterols impair lung macrophage phagocytosis via adduction of some phagocytosis receptors.

The Journal of Biological Chemistry
Parker F DuffneyIlona Jaspers

Abstract

Inhalation of the ambient air pollutant ozone causes lung inflammation and can suppress host defense mechanisms, including impairing macrophage phagocytosis. Ozone reacts with cholesterol in the lung to form oxysterols, like secosterol A and secosterol B (SecoA and SecoB), which can form covalent adducts on cellular proteins. How oxysterol-protein adduction modifies the function of lung macrophages is unknown. Herein, we used a proteomic screen to identify lung macrophage proteins that form adducts with ozone-derived oxysterols. Functional ontology analysis of the adductome indicated that protein binding was a major function of adducted proteins. Further analysis of specific proteins forming adducts with SecoA identified the phagocytic receptors CD206 and CD64. Adduction of these receptors with ozone-derived oxysterols impaired ligand binding and corresponded with reduced macrophage phagocytosis. This work suggests a novel mechanism for the suppression of macrophage phagocytosis following ozone exposure through the generation of oxysterols and the formation of oxysterol-protein adducts on phagocytic receptors.

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Citations

Jan 27, 2021·Free Radical Research·Sayuri MiyamotoLucas G Viviani
Nov 2, 2020·Archives of Biochemistry and Biophysics·Bianca S TakayasuJanice Onuki
Jun 16, 2021·American Journal of Respiratory Cell and Molecular Biology·Alexia PerrymanIlona Jaspers
Aug 11, 2021·American Journal of Respiratory Cell and Molecular Biology·Pedro HernandezAngela Haczku

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