Animal models of chronic bronchitis and their relevance to studies of particle-induced disease

Citation
Kj. Nikula et Fhy. Green, Animal models of chronic bronchitis and their relevance to studies of particle-induced disease, INHAL TOXIC, 12, 2000, pp. 123-153
Citations number
197
Categorie Soggetti
Pharmacology & Toxicology
Journal title
INHALATION TOXICOLOGY
ISSN journal
08958378 → ACNP
Volume
12
Year of publication
2000
Supplement
4
Pages
123 - 153
Database
ISI
SICI code
0895-8378(2000)12:<123:AMOCBA>2.0.ZU;2-#
Abstract
Chronic bronchitis is a significant cause of morbidity and mortality. Chron ic irritation of the conducting airways by inhaled substances, most importa ntly cigarette smoke, air pollution, and occupational exposures, is thought to be a key factor in the pathogenesis of chronic bronchitis. Microbial in fections have been implicated in acute exacerbations of bronchitis and in i ts progression. Several animal models of chronic bronchitis have been devel oped This review examines similarities and dissimilarities among commonly u sed animal models of bronchitis and the human disease. The most commonly us ed animal models of chronic bronchitis are those employing SO2, tobacco smo ke, lipopolysaccharide (endotoxin), pro ceases, and secretagogues. Bronchio litis induced by nickel and nitric acid have also been reported. Rats, hams ters, and dogs are the species most frequently used; sheep and monkeys have been used less frequently. These models vary in the extent or location of mucous-cell hyperplasia and metaplasia, airway inflammation, chronicity, ea se of induction, and reproducibility. Frequently, the deficiencies in these models are attributable to anatomic differences between human and animal a irways, differences in the severity or chronicity of inflammation or fibros is, or lack of complete characterization of the responses and their time co urse in the animal model. These animal models may be useful for investigati ng how, and under what exposure conditions, ambient pollutants might exacer bate airway inflammation, mucus hypersecretion, and airflow limitation.