Healthy volunteers underwent inhalation challenge to corn dust extract (CDE) and lipopolysaccharide (LPS) in an effort to enhance the understanding of the relationship between endotoxin and grain dust induced airway disease. The subjects included nine men and five women. They ranged in age from 20 to 48 years. The most common symptoms reported following inhalation exposure to both high and low endotoxin CDE and LPS solutions included chest tightness, cough, sputum production and dyspnea. Inhalation of LPS and CDE at high endotoxin concentrations resulted in a significant decline in 1 second forced expiratory volume (FEV1) from baseline beginning as early as 10 minutes after completion of exposure to both inhalants. The mean percentage declines in FEV1 from baseline in LPS exposed subjects were 17 to 19% and for CDE were 10 to 15% during the first 4 hours after exposure. Inhalation of high endotoxin LPS and CDE solutions resulted in an acute inflammatory response in the lung 4 hours after dosing. Greater concentrations of neutrophils were noted following exposure to LPS compared to CDE. Tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta, interleukin-6, and interleukin-8 concentrations were all increased in the bronchoalveolar lavage fluid 4 hours after dosing. Of the cytokines detected, only interleukin-6 was detected in the serum 4 hours after exposure at high and low endotoxin concentrations. TNF-alpha mRNA in BAL cells and interleukin-8 mRNA in airway epithelial cells were demonstrated after exposure. The authors conclude that endotoxin may be the primary mediator of airway inflammation in grain dust induced lung disease.
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