Title

Role of endotoxin in grain dust-induced lung inflammation in mice

Document Type

Article

Peer Reviewed

1

Publication Date

6-1-1996

Journal/Book/Conference Title

American Journal of Physiology: Lung Cellular and Molecular Physiology

Abstract

To investigate the role of endotoxin in grain dust-induced airway inflammation, we reduced the endotoxin activity from extracts of corn dust (CDE), using three distinct methods, and determined the effect of endotoxin activity on the in vitro and in vivo inflammatory response to CDE. Escherichia coli lipopolysaccharide solution (LPS) and CDE solution were separated into > 100-kDa and 100-kDa fractions of the LPS and CDE solutions. Charged-membrane filtration of the > 100-kDa fractions of LPS and CDE resulted in the reduction of endotoxin activity by 99.9 and 80%, respectively. Treatment of the > 100-kDa fractions of LPS and CDE with polymyxin B-coated beads reduced the endotoxin activity by 96 and 89%, respectively. The untreated > 100-kDa fractions of LPS and CDE caused significantly greater (P 100-kDa fractions of the LPS and CDE solutions. Charged-membrane filtration of the > 100-kDa fractions of LPS and CDE resulted in the reduction of endotoxin activity by 99.9 and 80%, respectively. Treatment of the > 100-kDa fractions of LPS and CDE with polymyxin B-coated beads reduced the endotoxin activity by 96 and 89%, respectively. The untreated > 100-kDa fractions of LPS and CDE caused significantly greater (P 100-kDa fractions. Similarly, mice exposed to either of the untreated > 100-kDa fractions of LPS or CDE by inhalation developed significantly greater (P 100-kDa fractions. Similarly, mice exposed to either of the untreated > 100-kDa fractions of LPS or CDE by inhalation developed significantly greater (P 100-kDa fractions. These results indicate that endotoxin is primarily responsible for the in vitro and in vivo inflammatory response to CDE.

Keywords

Sustainability

Published Article/Book Citation

American Journal of Physiology: Lung Cellular and Molecular Physiology, 270:6 (1996) pp.L1052-L1059.

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URL

https://ir.uiowa.edu/oeh_pubs/69