Nanoparticulate carbon black in cigarette smoke induces DNA cleavage and Th17-mediated emphysema

Ran You, Wen Lu, Ming Shan, Jacob M. Berlin, Errol L G Samuel, Daniela C. Marcano, Zhengzong Sun, William K A Sikkema, Xiaoyi Yuan, Lizhen Song, Amanda Y. Hendrix, James M. Tour, David B. Corry, Farrah Kheradmand

Research output: Contribution to journalArticle

33 Scopus citations

Abstract

Chronic inhalation of cigarette smoke is the major cause of sterile inflammation and pulmonary emphysema. The effect of carbon black (CB), a universal constituent of smoke derived from the incomplete combustion of organic material, in smokers and non-smokers is less known. In this study, we show that insoluble nanoparticulate carbon black (nCB) accumulates in human myeloid dendritic cells (mDCs) from emphysematous lung and in CD11c+ lung antigen presenting cells (APC) of mice exposed to smoke. Likewise, nCB intranasal administration induced emphysema in mouse lungs. Delivered by smoking or intranasally, nCB persisted indefinitely in mouse lung, activated lung APCs, and promoted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly in phagocytes. Increasing the polarity or size of CB mitigated many adverse effects. Thus, nCB causes sterile inflammation, DSB, and emphysema and explains adverse health outcomes seen in smokers while implicating the dangers of nCB exposure in non-smokers.

Original languageEnglish (US)
Article numbere09623
JournaleLife
Volume4
Issue numberOCTOBER2015
DOIs
StatePublished - Oct 5 2015

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology and Microbiology(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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