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Further, although several previous studies have evaluated GSH levels in various extracellular compartments, including bronchoalveolar lavage (BAL) fluid, these studies generally focused on alterations in GSH:GSSG balance in association with disease, or the consumption of GSH during prostaglandin or leukotriene synthesis, with more modest phenotypic, pathophysiologic, or mechanistic information (4, 5)

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Clarifying the stages at which these pathways contribute to the inflammatory phenotype and identifying the cell types orchestrating this inflammasome-independent response are crucial areas for further investigation