Treatment options for chronic inflammatory airway diseases are limited due to an incomplete understanding of the underlying pathomechanisms. In this thesis, metabolic- and immune cell profiles of patients with NSAID-exacerbated respiratory disease (N-ERD), a severe type 2 inflammatory condition, were characterized by multi-omics approaches. N-ERD macrophages displayed a persistent, pro-inflammatory phenotype, which was associated with local and systemic lipid metabolism alterations. Our study suggests that pro-inflammatory macrophage reprogramming is a pathomechanism of N-ERD.
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Treatment options for chronic inflammatory airway diseases are limited due to an incomplete understanding of the underlying pathomechanisms. In this thesis, metabolic- and immune cell profiles of patients with NSAID-exacerbated respiratory disease (N-ERD), a severe type 2 inflammatory condition, were characterized by multi-omics approaches. N-ERD macrophages displayed a persistent, pro-inflammatory phenotype, which was associated with local and systemic lipid metabolism alterations. Our study su...
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