Particulate matter air pollution from the city of Quito, Ecuador, activates inflammatory signaling pathways in vitro

Innate Immun. 2017 May;23(4):392-400. doi: 10.1177/1753425917699864. Epub 2017 Mar 21.

Abstract

Automobile traffic, industrial processes and natural phenomena cause notable air pollution, including gaseous and particulate contaminants, in urban centers. Exposure to particulate matter (PM) air pollution affects human health, and has been linked to respiratory, cardiovascular and neurological diseases. The mechanisms underlying inflammation in these diverse diseases, and to what extent health effects are different for PM obtained from different sources or locations, are still unclear. This study investigated the in vitro toxicity of ambient course (PM10) and fine (PM2.5) particulate matter collected at seven sites in the urban and periurban zones of Quito, Ecuador. Material from all sites was capable of activating TLR2 and TLR4 signaling pathways, with differences in the activation related to particle size. Additionally, airborne particulate matter from Quito is an effective activator of the NLRP3 inflammasome.

Keywords: LPS; NLRP3 inflammasome; TLR2; TLR4; particulate matter.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ecuador
  • HEK293 Cells
  • Humans
  • Inflammasomes / metabolism
  • Inflammation / immunology*
  • Macrophages / immunology*
  • Mice
  • Mice, Inbred C57BL
  • NLR Family, Pyrin Domain-Containing 3 Protein / metabolism*
  • Particle Size
  • Particulate Matter / immunology*
  • Signal Transduction
  • Toll-Like Receptor 2 / metabolism*
  • Toll-Like Receptor 4 / metabolism*

Substances

  • Inflammasomes
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Nlrp3 protein, mouse
  • Particulate Matter
  • TLR2 protein, human
  • TLR4 protein, human
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4