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1 Departement de Pneumologie Pediatrique-Institut National de la Santé et de la Recherche Médicale E213, Hopital Armand Trousseau, 75012 Paris; and 2 Unite Postulante Cytokines and Inflammation, Institut Pasteur, 75015 Paris, France
Inflammation plays a critical role
in lung disease progression in cystic fibrosis (CF). This inflammatory
process is dominated by a neutrophil influx in the airways. To
determine whether the accumulation of neutrophils in the airways of CF
patients is associated with an altered function, we analyzed the
capacity of neutrophils isolated from the lung compartment and the
blood to release the major neutrophil pro- and anti-inflammatory
cytokines IL-8 and IL-1-receptor antagonist (ra) spontaneously and in
the presence of LPS. Comparison of cytokine production by blood
neutrophils from CF patients and from control subjects showed
significantly increased IL-8 and decreased IL-1ra release by CF
neutrophils. Comparison of cytokine production by airway and blood
neutrophils from CF patients also documented distinct profiles: the
spontaneous release of IL-8 and IL-1ra by airway neutrophils was
significantly higher than that from blood neutrophils. Culture in the
presence of LPS failed to further enhance cytokine production. Analysis of the effect of dexamethasone confirmed the difference in the responsiveness of lung and blood neutrophils in CF. Used at a concentration effective in reducing IL-8 production by blood
neutrophils, dexamethasone (10
6 M) was unable to repress
secretion of IL-8 by airway neutrophils. In addition, comparison of
cytokine production by airway neutrophils from children with CF and
children with dyskinetic cilia syndrome also documented distinct
profiles of secretion. These results are consistent with a dysregulated
cytokine production by lung and blood neutrophils in CF. They provide
support to the hypothesis that not only the CF genotype but also the
local environment may modify the functional properties of the neutrophils.
inflammation; cytokines
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