The pulmonary effects of a bacterial endotoxin were studied in guinea-pigs. English-short-hair-guinea-pigs were exposed to 0 or 10 micrograms per milliliter aerosols of endotoxin from Pantoea- agglomerans or a saline extract of the bacteria for 3 hours. Controls breathed saline aerosols or filtered air. Breathing rates were monitored for up to 18 hours post exposure by whole body plethysmography. The animals were then killed and the lungs were removed and lavaged. Changes in lavagate cellularity were determined. Alveolar macrophages were recovered from the lavagate and examined for morphological changes by electron microscopy. Resting and phorbol-myristate-acetate (PMA) and zymosan stimulated production of superoxide anion (O2-) by the macrophages was determined. Inhalation of P-agglomerans endotoxin and the saline extract increased the breathing rate by 37 and 62%, respectively, which were statistically significant increases. Both preparations caused significant increases in lavage fluid total cellularity and alveolar macrophage, neutrophil, lymphocyte, and red blood cell counts. Control macrophages typically had smooth surfaces and small pseudopodia. Macrophages from exposed guinea-pigs had rough sides and showed blebbing, filopodia, and surface ruffling. Alveolar macrophages recovered from control animals showed low levels of basal O2- production. Macrophages from endotoxin or bacterial extract treated animals showed significant increases in basal and PMA and zymosan stimulated O2- production. The increases were much higher in macrophages obtained from endotoxin exposed animals. The author concludes that inhalation of P-agglomerans endotoxin increases respiratory rates and pulmonary influx of inflammatory cells and spontaneous and PMA and zymosan stimulated release of O2- from alveolar macrophages. These results and those of previous studies indicate that inhalation of Gram negative bacteria can induce pathogenic responses in agricultural workers.
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