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American Journal of Pathology, Vol 130, 605-615, Copyright © 1988 by American Society for Investigative Pathology
REGULAR ARTICLES |
JR Harkema, JA Hotchkiss, AG Harmsen and RF Henderson
Lovelace Inhalation Toxicology Research Institute, Albuquerque, NM 87185.
Certain inhaled toxicants are known to induce mucous hypersecretion in the respiratory epithelium. This secretory change may be a direct effect of the toxicant or an indirect effect of the concomitant inflammatory response. The present study was designed to determine by quantitative histochemistry whether the influx of neutrophils through the nasal respiratory epithelium would induce significant quantitative changes in the amount of intraepithelially stored mucosubstance. F344/N rats were intranasally instilled with endotoxin to elicit a transient influx of neutrophils into the nasal epithelium. Peak intraepithelial infiltration of neutrophils was evident 6 hours after instillation. There was a concurrent quantitative decrease in stored epithelial mucosubstance at the same time after instillation. Amounts of epithelial mucosubstance returned to that measured prior to neutrophil infiltration by 24 hours after instillation, when intraepithelial neutrophils were diminishing. Rats in which circulating neutrophils were sequestered in the lungs and prevented from migrating into endotoxin-exposed nasal epithelium had no change in the quantity of stored mucosubstance 6 hours after instillation. Therefore, it is concluded that a transepithelial migration of neutrophils elicits a transient depletion of stored mucosubstances in the nasal respiratory epithelium. Whether this is due to the release of secretagogues from the migrating leukocytes or another neutrophil-related method of stimulating mucous secretion is not known.
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