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Granulocyte recruitment to airways exposed to endotoxin aerosols.

作者信息

Hudson A R, Kilburn K H, Halprin G M, McKenzie W N

出版信息

Am Rev Respir Dis. 1977 Jan;115(1):89-95. doi: 10.1164/arrd.1977.115.1.89.

DOI:10.1164/arrd.1977.115.1.89
PMID:835896
Abstract

Guinea pigs were exposed to aerosols of 0.1 mg of Salmonella typhosa endotoxin per ml for 2 or 4 hours, and white cells in blood and in bronchopulmonary lavage were counted at 2, 4, and 6 hours. The lungs of a second group of guinea pigs and hamsters exposed in the same manner were fixed in inflation with osmium tetroxide in fluorocarbon, which retains cells on luminal surfaces of airways. The polymorphonuclear leukocyte counts in cardiac blood were significantly increased, and lymphocyte counts were decreased at 6 hours (P less than 0.05). The number of cells obtained by bronchopulmonary lavage, which were mostly polymorphonuclear leukocytes, increased at 4 hours to 28 million, and at 6 hours, was 26.5 million (P less than 0.01), compared to 5 million cells at the same times in air and in water aerosol control preparations. The polymorphonuclear cell counts on airway cross sections, i.e., (polymorphonuclear cells/epithelial cells) x 100, showed a mean +/- SD peak of 53.9 +/- 10.9 after 4 hours in guinea pigs and a peak of 99.7 +/- 11.0 after 6 hours in hamsters. Alveoli showed no cell recruitment. Platelets were aggregated on surfaces of arterioles facing bronchioles, although counts in blood were unchanged. Neither leukocytes nor airway cells showed damage to their ultrastructure. The time course for airway recruitment and leukocytosis matches that for symptoms after exposure of workers to dusts from natural fodder or fibers. This suggests that leukocyte recruitment to airways by inhaled endotoxin may be part of the mechanism for the fever and chest tightness in occupational disorders.

摘要

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