1. Human Biology and Medicine
  2. Immunology and Inflammation
Download icon

Lung Disease: The soot of all evil

  1. Derek W Russell
  2. J Edwin Blalock  Is a corresponding author
  1. University of Alabama at Birmingham, United States
Insight
Cite this article as: eLife 2015;4:e11709 doi: 10.7554/eLife.11709
1 figure

Figures

Nanocarbon black triggers perpetual inflammation in the lung.

Nanoparticles of carbon black are consumed by antigen-presenting cells, such as human myeloid dendritic cells, where they lead to DNA breaks. This, in turn, initiates the activation of a complex of proteins called the inflammasome, which includes the Caspase-1 protein (Taniguchi and Sagara, 2007). The activated inflammasome leads to the cleavage of Pro-IL1β to make a mature signal protein called IL-1β, while also initiating processes that will lead to the death of the cell. The mature IL-1β causes upregulation of several inflammatory pathways, including the increased transcription of IL-6. These cytokines then act together to trigger T lymphocytes to become T helper 17 (TH17) cells. These cells produce the inflammatory cytokine IL-17, which has been implicated in chronic obstructive pulmonary disease. When the antigen-presenting cell dies, the nanoparticles are released to be taken up by another generation of antigen-presenting cells, which lead to another cycle of inflammation. IL = interleukin; ASC = Adaptor Protein Apoptosis-Associated Speck-Like Protein Containing CARD.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Download citations (links to download the citations from this article in formats compatible with various reference manager tools)

Open citations (links to open the citations from this article in various online reference manager services)