Premium
Murine Model of Occupational Injury Induced by Chronic Exposure to Oak Dust
Author(s) -
McClintock Shan D.,
Barron Adam,
Warner Roscoe L.,
Johnson Kent J.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.710.10
Subject(s) - hypersensitivity pneumonitis , medicine , chronic bronchitis , inhalation , particulates , population , phagocytosis , lung , asthma , alveolar macrophage , inhalation exposure , inflammation , pathology , immunology , macrophage , chemistry , environmental health , anesthesia , biochemistry , organic chemistry , in vitro
Chronic exposure to airborne particulates is well described as the primary cause of occupational pulmonary injury and increases the risk of asthma, chronic bronchitis, allergic rhinitis and hypersensitivity pneumonitis. Sources of both inorganic and organic particulates are derived of bacterial, fungal, chemical, plant, or animal origin. While inhalation of wood dust of several particulate sizes has long been thought of as an occupational hazard for those in the woodworking industry it has not been directly implicated as the causative agent for pulmonary injury. Herein we present a mouse model of chronic exposure to wood dust resulting in a pneumonitis type injury. Intratracheal administration of an oak dust suspension (80 micro‐L) was performed three times per week for four weeks. Histological examination demonstrated an influx of inflammatory cells peri‐airway and a resident macrophage population swollen to several times their normal size, due in part to the phagocytosis of particulates. Increased interstitial thickening of the smaller airways and alveolar compartments were noted in the lungs of injured mice relative to uninjured controls. Results from these experiments demonstrate that repeated exposure to oak dust induces lung inflammation and a pneumonitis type injury and may offer a model to better understanding and subsequently treat occupational pulmonary injury. Work supported by NIH RO1 HL07097