Exposure to biomass smoke extract enhances fibronectin release from fibroblasts

David Krimmer, Yukikazu Ichimaru, Janette Burgess, Judith Black, Brian Oliver

Research output: Contribution to journalArticleAcademicpeer-review

32 Citations (Scopus)
25 Downloads (Pure)

Abstract

COPD induced following biomass smoke exposure has been reported to be associated with a more fibrotic phenotype than cigarette smoke induced COPD. This study aimed to investigate if biomass smoke induced extracellular matrix (ECM) protein production from primary human lung fibroblasts in vitro. Primary human lung fibroblasts (n = 5-10) were stimulated in vitro for up to 72 hours with increasing concentrations of biomass smoke extract (BME) or cigarette smoke extract (CSE) prior to being assessed for deposition of ECM proteins, cytokine release, and activation of intracellular signalling molecules. Deposition of the ECM proteins perlecan and fibronectin was upregulated by both CSE (p,0.05) and BME (p,0.05). The release of the neutrophilic chemokine IL-8 was also enhanced by BME. ERK1/2 phosphorylation was significantly upregulated by BME (p,0.05). Chemical inhibition of ERK signalling molecules partially attenuated these effects (p,0.05). Stimulation with endotoxin had no effect. This study demonstrated that BME had similar effects to CSE in vitro and had the capacity to directly induce fibrosis by upregulating production of ECM proteins. The mechanisms by which both biomass and cigarette smoke exposure cause lung damage may be similar. Copyright: © 2013 Krimmer et a.
Original languageEnglish
Article numbere83938
Number of pages10
JournalPLoS ONE
Volume8
Issue number12
DOIs
Publication statusPublished - 26-Dec-2013
Externally publishedYes

Keywords

  • biofuel
  • biomass smoke extract
  • cigarette smoke
  • endotoxin
  • fibronectin
  • interleukin 8
  • perlecan
  • scleroprotein
  • toxic substance
  • unclassified drug
  • adult
  • aged
  • article
  • cell activation
  • concentration (parameters)
  • controlled study
  • cytokine release
  • cytotoxicity
  • enzyme inhibition
  • exposure
  • extracellular matrix
  • female
  • fibroblast
  • human
  • human cell
  • human tissue
  • in vitro study
  • lung injury
  • male
  • protein phosphorylation
  • protein secretion
  • upregulation
  • very elderly

Cite this