Administering recombinant interleukin-1 beta (IL-1 beta) intratracheal
ly caused lung neutrophil accumulation and lung injury in hamsters. Th
e percentage of leukocytes that were neutrophils increased progressive
ly in lavages from lungs of hamsters given 25, 50, or 100 ng IL-1 beta
intratracheally 2 h before. Lung injury, reflected by increased lung
lavage protein concentrations and lung lavage hemoglobin concentration
s, increased 2 h after administering 100 ng IL-1 beta. Lung injury, re
flected by lung wet weight/body weight ratios, followed similar patter
ns, with significant increases occurring 2 h after insufflating 50 or
100 ng IL-1. Our results indicate that increased concentrations of IL-
1 beta in lung airways can cause neutrophil recruitment and lung injur
y in hamsters. This mechanism may contribute to the development of lun
g neutrophil accumulation and lung injury that characterizes ARDS pati
ents who have increased airway levels of IL-1 beta.