Chronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung cancer.

ABSTRACT: Chronic exposure to airborne carbon black ultrafine (nCB) particles generated from incomplete combustion of organic matter drives IL-17A-dependent emphysema. However, whether and how they alter the immune responses to lung cancer remains unknown. Here, we show that exposure to nCB particles increased PD-L1⁺ PD-L2⁺ CD206⁺ antigen-presenting cells (APCs), exhausted T cells, and T_reg cells. Lung macrophages that harbored nCB particles showed selective mitochondrial structure damage and decreased oxidative respiration. Lung macrophages sustained the HIF1α axis that increased glycolysis and lactate production, culminating in an immunosuppressive microenvironment in multiple mouse models of non-small cell lung cancers. Adoptive transfer of lung APCs fr

SUBMITTER: Chang CY 

PROVIDER: S-EPMC9668323 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature