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Am. J. Respir. Crit. Care Med., Volume 158, Number 6, December 1998, 1702-1708

Protective Effect of Endotoxin Instillation on Subsequent Bacteria-induced Acute Lung Injury in Rats

DANIEL JEAN, SAÏDA REZAIGUIA-DELCLAUX, CHRISTOPHE DELACOURT, ROLAND LECLERCQ, CHANTAL LAFUMA, CHRISTIAN BRUN-BUISSON, ALAIN HARF, and CHRISTOPHE DELCLAUX

Institut National de la Santé et de la Recherche Médicale, INSERM U 296; Service d'Anesthésie-Réanimation, Service de Bactériologie, Service de Réanimation Médicale, and Service de Physiologie, Hôpital Henri Mondor, Créteil; and Clinique Équine, DEPEC, Ecole Vétérinaire d'Alfort, Maisons-Alfort, France

The phagocytic capability afforded by neutrophil influx into the lungs is essential to ward off invading bacteria. The objective of this study was to evaluate the effect of prior neutrophil recruitment induced by alveolar instillation of endotoxin (LPS, 200 µg/kg) 16 h before a pulmonary infection caused by instillation of live Pseudomonas aeruginosa ([PYO]: 1.5 × 108 colony-forming units [cfu]/kg) in rats. A first series of experiments showed that lipopolysaccharide (LPS) instillation induced recruitment of alveolar neutrophils that were capable, ex vivo, of elastase exocytosis, reactive oxygen species secretion, and PYO killing. In a second set of experiments, LPS followed by PYO was compared with PYO alone (n = 11 surviving rats in each group). Parameters were studied 24 h after the bacterial challenge. As compared with PYO alone, pretreatment with LPS followed by PYO was associated with decreased mortality (0% versus 54%, p < 0.05), decreased protein leakage into bronchoalveolar lavage (BAL) fluid (1.8 ± 0.4 versus 13.5 ± 2.2 mg/ml, p < 0.001), and improved bacterial clearance from BAL (4.0 ± 1.4 × 102 versus 1.2 ± 0.5 × 104 cfu/ml, p < 0.05) and from pulmonary parenchyma (8.5 ± 6.4 × 105 versus 1.9 ± 0.8 × 107 cfu/ml, p < 0.05). We conclude that prior alveolar endotoxin instillation induces local recruitment of functionally active neutrophils, and that this is associated with resistance to subsequent experimental pneumonia.




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Copyright © 1998 American Thoracic Society