Research ArticleLUNG DISEASE

Itaconate controls the severity of pulmonary fibrosis

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Science Immunology  23 Oct 2020:
Vol. 5, Issue 52, eabc1884
DOI: 10.1126/sciimmunol.abc1884

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Itaconate in fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease associated with accumulation of extracellular matrix in the lung. Here, Ogger et al. define a role for itaconate in regulating fibrosis. Itaconate synthesis by macrophages is catalyzed by cis-aconitate decarboxylase, which is encoded by aconitate decarboxylase 1 (ACOD1). Itaconate levels are lower in bronchoalveolar lavage, and ACOD1 expression is decreased in alveolar macrophages (AMs) of patients with IPF compared with controls. Acod1−/− mice develop severe pulmonary fibrosis relative to wild-type (WT) littermates, and adoptive transfer of WT, but not Acod1−/−, Mo-AMs into Acod1−/− mice rescued the fibrotic phenotype. Treatment of Acod1−/− mice with inhaled itaconate also had an antifibrotic effect. These findings highlight a role for itaconate in controlling lung fibrosis, revealing a pathway for potential therapeutics.

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