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1 Hopital Armand Trousseau, Departement de Pneumologie Pediatrique - INSERM E0213, Paris, France
2 Institut Pasteur, UP Cytokines et Inflammation, Paris, France
* To whom correspondence should be addressed. E-mail: annick.clement{at}trs.ap-hop-paris.fr.
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 from the blood to release the major neutrophil pro and anti-inflammatory cytokines, interleukin (IL)-8 and IL-1ra, spontaneously and in the presence of lipopolysaccharide (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 airways and blood neutrophils from CF patients also documented distinct profiles : the spontaneous release of IL-8 and IL-1ra by airways 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 airways neutrophils. In addition, comparison of cytokine production by airways neutrophils from CF children and from 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.
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