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

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dc.citation.articleNumbereabq0615en_US
dc.citation.issueNumber46en_US
dc.citation.journalTitleScience Advancesen_US
dc.citation.volumeNumber8en_US
dc.contributor.authorChang, Cheng-Yenen_US
dc.contributor.authorYou, Ranen_US
dc.contributor.authorArmstrong, Dominiqueen_US
dc.contributor.authorBandi, Ashwinien_US
dc.contributor.authorCheng, Yi-Tingen_US
dc.contributor.authorBurkhardt, Philip M.en_US
dc.contributor.authorBecerra-Dominguez, Luisen_US
dc.contributor.authorMadison, Matthew C.en_US
dc.contributor.authorTung, Hui-Yingen_US
dc.contributor.authorZeng, Zhiminen_US
dc.contributor.authorWu, Yifanen_US
dc.contributor.authorSong, Lizhenen_US
dc.contributor.authorPhillips, Patricia E.en_US
dc.contributor.authorPorter, Paulen_US
dc.contributor.authorKnight, John M.en_US
dc.contributor.authorPutluri, Nagireddyen_US
dc.contributor.authorYuan, Xiaoyien_US
dc.contributor.authorMarcano, Daniela C.en_US
dc.contributor.authorMcHugh, Emily A.en_US
dc.contributor.authorTour, James M.en_US
dc.contributor.authorCatic, Andreen_US
dc.contributor.authorManeix, Laureen_US
dc.contributor.authorBurt, Bryan M.en_US
dc.contributor.authorLee, Hyun-Sungen_US
dc.contributor.authorCorry, David B.en_US
dc.contributor.authorKheradmand, Farrahen_US
dc.date.accessioned2022-12-13T19:11:39Zen_US
dc.date.available2022-12-13T19:11:39Zen_US
dc.date.issued2022en_US
dc.description.abstractChronic 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 Treg 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 from nCB-exposed wild type to susceptible mice increased tumor incidence and caused early metastasis. Our findings show that nCB exposure metabolically rewires lung macrophages to promote immunosuppression and accelerates the development of lung cancer.en_US
dc.identifier.citationChang, Cheng-Yen, You, Ran, Armstrong, Dominique, et al.. "Chronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung cancer." <i>Science Advances,</i> 8, no. 46 (2022) AAAS: https://doi.org/10.1126/sciadv.abq0615.en_US
dc.identifier.digitalsciadv-abq0615en_US
dc.identifier.doihttps://doi.org/10.1126/sciadv.abq0615en_US
dc.identifier.urihttps://hdl.handle.net/1911/114130en_US
dc.language.isoengen_US
dc.publisherAAASen_US
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license, which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited.en_US
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/en_US
dc.titleChronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung canceren_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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