title: Exposure to biomass smoke extract enhances fibronectin release from fibroblasts.
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.
authors.affiliation: The Woolcock Institute of Medical Research, Sydney, Australia ; The Discipline of Pharmacology, University of Sydney, Sydney, Australia.
authors.forename: David
authors.initials: D
authors.lastname: Krimmer
authors.affiliation: The Woolcock Institute of Medical Research, Sydney, Australia ; The Discipline of Pharmacology, University of Sydney, Sydney, Australia.
authors.forename: Yukikazu
authors.initials: Y
authors.lastname: Ichimaru
authors.affiliation: The Woolcock Institute of Medical Research, Sydney, Australia ; The Discipline of Pharmacology, University of Sydney, Sydney, Australia.
authors.forename: Janette
authors.initials: J
authors.lastname: Burgess
authors.affiliation: The Woolcock Institute of Medical Research, Sydney, Australia ; The Discipline of Pharmacology, University of Sydney, Sydney, Australia.
authors.forename: Judith
authors.initials: J
authors.lastname: Black
authors.affiliation: The Woolcock Institute of Medical Research, Sydney, Australia ; The Discipline of Pharmacology, University of Sydney, Sydney, Australia.
authors.forename: Brian
authors.initials: B
authors.lastname: Oliver
mesh_terms: D000328:Adult; D000368:Aged; D056151:Airway Remodeling / Q000187:drug effects; D018533:Biomass; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors; D005260:Female; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism*; D005353:Fibronectins / Q000378:metabolism*; D005541:Forced Expiratory Volume / Q000187:drug effects; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010766:Phosphorylation / Q000187:drug effects; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D012906:Smoke / Q000009:adverse effects*; D062789:Tobacco Products / Q000032:analysis
chemical_list: D005353:Fibronectins; D016209:Interleukin-8; D047428:Protein Kinase Inhibitors; D012906:Smoke; D048049:Extracellular Signal-Regulated MAP Kinases