Although thickening of the subepithelial region of the airway is a consistent feature in the cellular structure of asthma, cystic fibrosis, and chronic obstructive lung disease and is directly related to the clinical severity of these diseases, the biological factors that lead to a localized fibrotic response following chronic airway inflammation have not been well defined.
To elucidate whether neutrophils are essential to the development of chronic LPS-induced airway disease, researchers used PMN antiserum to produce neutrophil-depleted mice and examined the LPS-induced changes in those animals compared to similarly exposed mice that were not neutropenic.
The researchers hypothesized that antiserum to PMNs would substantially minimize the acute inflammatory response to inhaled LPS and in doing so would substantially inhibit subepithelial thickening and alter the development of chronic LPS-induced airway disease.
The authors of "Neutrophils Play a Critical Role in Development of LPS-Induced Airway Disease," are Jordan D. Savov, David M. Brass and David A. Schwartz, all from the Pulmonary and Critical Care Division, Department of Medicine, Duke University Medical Center and Veterans Affairs Medical Center, Durham, NC. Additional authors are Stephen H. Gavett and Daniel L. Costa, both from the Pulmonary Toxicology Branch, Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, United States E
Contact: Donna Krupa
American Physiological Society