ISSN:
1573-2592
Keywords:
Alveolar macrophage
;
shock
;
endotoxin
;
tumor necrosis factor
;
interleukin-1
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract To elucidate potential mechanisms of the acute lung injury associated with endotoxemia, we evaluated the effect of intravenously administered endotoxin on the ability of alveolar macrophages isolated by bronchoalveolar lavage from normal subjects to produce inflammatory mediators. Within 1 hr of endotoxin (4 ng/kg body weight) administration, all 12 study subjects developed constitutional symptoms and leukopenia, and within 3 hr, lowgrade fever. Resolution of symptoms and fever by 6 hr was accompanied by systemic granulocytosis. Although intravenously administered endotoxin appeared to activate a subset of circulating monocytes, it did not alter the bronchoalveolar lavage cell number, phenotype (95% macrophages), or constitutively expressed high levels of surface HLA-DR and O 2 − . In contrast, intravenous endotoxin primed the alveolar macrophages for enhanced lipopolysaccharide-induced secretion of interleukin-1 (11.8 to 25.8 U/ml;P=0.04), tumor necrosis factor-α (titer, 6.8 to 13.6;P=0.20), and prostaglandin E2 (38.4 to 116.3 ng/ml;P=0.035). These results demonstrate that low-dose intravenous endotoxin primes human alveolar macrophages, which are already differentiatedin situ, for enhanced secretion of inflammatory mediators. Such mediators may contribute to the pulmonary changes associated with endotoxemia and acute lung injury.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01541347
