Am. J. Respir. Crit. Care Med., Vol 153, No. 1, Jan 1996, 336-342.
Compartmentalized IL-8 and elastase release within the human lung in unilateral pneumonia
A Boutten, MS Dehoux, N Seta, J Ostinelli, P Venembre, B Crestani, MC Dombret, G Durand and M Aubier
Services de Biochimie A et de Pneumologie, INSERM U408, Hopital Bichat, Paris, France.
Because interleukin 8 (IL-8) is a potent neutrophil chemotactic and
activating cytokine, we investigated IL-8 production in relation to
neutrophil migration and elastase release in the human lung during
unilateral community-acquired pneumonia (CAP). In 17 patients, the local
response in the involved lung was compared with that in the contralateral,
noninvolved lung, and with the systemic response. Eight healthy volunteers
served as controls. IL-8, total neutrophil elastase (NE), free elastase
activity, alpha 1-antitrypsin (alpha 1-AT), and total leukocyte and
neutrophil counts were evaluated in bronchoalveolar lavage fluids (BALF).
Mean IL-8 concentrations in BALF from the involved lungs of the patients
were significantly greater than those in BALF from the noninvolved lung or
from controls (p < or = 0.001). By contrast, the serum IL-8
concentration was not different in patients and in controls. Total NE and
alpha 1-AT concentrations were increased in BALF from the involved lung as
compared with the noninvolved lung or controls (p < or = 0.001). The
elastase-inhibitory capacity of alpha 1- AT in BALF was impaired in the
involved lung of seven of the 14 patients as compared with the controls,
leading to free elastase activity in the involved lung of all patients with
CAP. Plasma total NE concentrations were significantly greater in the CAP
patients than in the controls. IL-8 concentrations in BALF correlated
positively with total leukocyte counts, absolute numbers and percentages of
neutrophils, total NE concentrations, and free elastase activity. Our
results suggest that during unilateral CAP, locally produced IL-8 may
trigger neutrophil accumulation and activation, thus contributing to a
local elastase/antielastase imbalance within the site of infection.
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Copyright © 1996 American Thoracic Society
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