Dung biomass smoke activates inflammatory signaling pathways in human small airway epithelial cells.
Animal dung is a biomass fuel burned by vulnerable populations who cannot afford cleaner sources of energy, such as wood and gas, for cooking and heating their homes. Exposure to biomass smoke is the leading environmental risk for mortality, with over 4,000,000 deaths each year worldwide attributed to indoor air pollution from biomass smoke. Biomass smoke inhalation is epidemiologically associated with pulmonary diseases, including chronic obstructive pulmonary disease (COPD), lung cancer, and respiratory infections, especially in low and middle-income countries. Yet, few studies have examined the mechanisms of dung biomass smoke-induced inflammatory responses in human lung cells. Here, we tested the hypothesis that dung biomass smoke causes inflammatory responses in human lung cells through signaling pathways involved in acute and chronic lung inflammation. Primary human small airway epithelial cells (SAECs) were exposed to dung smoke at the air-liquid interface using a newly developed, automated, and reproducible dung biomass smoke generation system. The examination of inflammatory signaling showed that dung biomass smoke increased the production of several proinflammatory cytokines and enzymes in SAECs through activation of the activator protein (AP)-1 and arylhydrocarbon receptor (AhR) but not nuclear factor-κB (NF-κB) pathways. We propose that the inflammatory responses of lung cells exposed to dung biomass smoke contribute to the development of respiratory diseases.
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.|Lung Biology and Disease Program, University of Rochester, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Claire E
CE
McCarthy
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.|Lung Biology and Disease Program, University of Rochester, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Parker F
PF
Duffney
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Robert
R
Gelein
Division of Pulmonary and Critical Care Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York; and.|Lung Biology and Disease Program, University of Rochester, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Thomas H
http://orcid.org/0000-0001-7177-3041
TH
Thatcher
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.|Lung Biology and Disease Program, University of Rochester, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Alison
A
Elder
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York.|Division of Pulmonary and Critical Care Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York; and.|Lung Biology and Disease Program, University of Rochester, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Richard P
RP
Phipps
Department of Environmental Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York; Patricia_Sime@urmc.rochester.edu.|Division of Pulmonary and Critical Care Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York; and.|Lung Biology and Disease Program, University of Rochester, University of Rochester School of Medicine and Dentistry, Rochester, New York.
Patricia J
PJ
Sime
D000818:Animals; D001391:Azo Compounds / Q000494:pharmacology; D018533:Biomass; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D006736:Horses; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008168:Lung / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D052638:Particulate Matter / Q000032:analysis; D011720:Pyrazoles / Q000494:pharmacology; D018336:Receptors, Aryl Hydrocarbon / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D012906:Smoke / Q000009:adverse effects*; D018808:Transcription Factor AP-1 / Q000378:metabolism
C511621:2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazophenyl)amide; D001391:Azo Compounds; D016207:Cytokines; D016328:NF-kappa B; D052638:Particulate Matter; D011720:Pyrazoles; D018336:Receptors, Aryl Hydrocarbon; D012906:Smoke; D018808:Transcription Factor AP-1; D051546:Cyclooxygenase 2; D048031:JNK Mitogen-Activated Protein Kinases
biomass smoke; inflammatory responses; particulates; respiratory toxicology; small airway epithelial cells