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1Department of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham 27710-0001; and 2United States Environmental Protection Agency, National Health and Environmental Effects Research Laboratory, Research Triangle Park, North Carolina 27711
Submitted 6 January 2003 ; accepted in final form 27 May 2003
The endotoxin component of organic dusts causes acute reversible airflow
obstruction and airway inflammation. To test the hypothesis that endotoxin
alone causes airway remodeling, we have compared the response of two inbred
mouse strains to subchronic endotoxin exposure. Physiological and biological
parameters were evaluated after 1 day, 5 days, or 8 wk of exposure to
endotoxin [lipopolysaccharide (LPS)] in endotoxin-sensitive (C3HeB/FeJ) and
endotoxin-resistant (C3H/HeJ) mice. After 5 days or 8 wk of LPS exposure, only
C3HeB/FeJ had elevated airway hyperreactivity to inhaled methacholine. Only
the C3HeB/FeJ mice had significant inflammation of the lower respiratory tract
after 1 day, 5 days, or 8 wk of LPS exposure. Stereological measurements of
small, medium, and large airways indicated that an 8-wk exposure to LPS
resulted in expansion of the submucosal area only in the C3HeB/FeJ mice. Cell
proliferation as measured by bromodeoxyuridine incorporation contributed to
the expansion of the submucosa and was only significantly elevated in
C3HeB/FeJ mice actively exposed to LPS. C3HeB/FeJ mice had significantly
elevated levels of interleukin-1
protein in whole lung lavage after 1
day and 5 days of LPS exposure and significantly elevated protein levels of
total and active transforming growth factor-1 in whole lung lavage fluid
after 5 days of LPS exposure. Our findings demonstrate that subchronic
inhalation of LPS results in the development of persistent airway disease in
endotoxin-responsive mice.
airway remodeling; neutrophilic inflammation; cytokines
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