Electronic cigarette exposure triggers neutrophil inflammatory responses

Respir Res. 2016 May 17;17(1):56. doi: 10.1186/s12931-016-0368-x.


Background: The use of electronic cigarettes (e-cigs) is increasing and there is widespread perception that e-cigs are safe. E-cigs contain harmful chemicals; more research is needed to evaluate the safety of e-cig use. Our aim was to investigate the effects of e-cigs on the inflammatory response of human neutrophils.

Methods: Neutrophils were exposed to e-cig vapour extract (ECVE) and the expression of CD11b and CD66b was measured by flow cytometry and MMP-9 and CXCL8 by ELISA. We also measured the activity of neutrophil elastase (NE) and MMP-9, along with the activation of inflammatory signalling pathways. Finally we analysed the biochemical composition of ECVE by ultra-high performance liquid chromatography mass spectrometry.

Results: ECVE caused an increase in the expression of CD11b and CD66b, and increased the release of MMP-9 and CXCL8. Furthermore, there was an increase in NE and MMP-9 activity and an increase in p38 MAPK activation. We also identified several harmful chemicals in ECVE, including known carcinogens.

Conclusions: ECVE causes a pro-inflammatory response from human neutrophils. This raises concerns over the safety of e-cig use.

Keywords: COPD; Electronic cigarettes; Inflammation; MMP-9; Neutrophils; Smoking.

MeSH terms

  • Antigens, CD / metabolism
  • CD11b Antigen / metabolism
  • Cell Adhesion Molecules / metabolism
  • Cells, Cultured
  • Consumer Product Safety
  • Dose-Response Relationship, Drug
  • Electronic Nicotine Delivery Systems*
  • GPI-Linked Proteins / metabolism
  • Humans
  • Inflammation / chemically induced*
  • Inflammation / immunology
  • Inflammation / metabolism
  • Interleukin-8 / metabolism
  • Leukocyte Elastase / metabolism
  • Matrix Metalloproteinase 9 / metabolism
  • Neutrophil Activation / drug effects*
  • Neutrophils / drug effects*
  • Neutrophils / immunology
  • Neutrophils / metabolism
  • Nicotinic Agonists / toxicity*
  • Risk Assessment
  • Signal Transduction / drug effects
  • Vaping / adverse effects*
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Antigens, CD
  • CD11b Antigen
  • CEACAM8 protein, human
  • CXCL8 protein, human
  • Cell Adhesion Molecules
  • GPI-Linked Proteins
  • ITGAM protein, human
  • Interleukin-8
  • Nicotinic Agonists
  • p38 Mitogen-Activated Protein Kinases
  • Leukocyte Elastase
  • MMP9 protein, human
  • Matrix Metalloproteinase 9