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Anti-inflammatory cytokines in cystic fibrosis lung disease

¹ Lung Research Group, Children's Hospital of Ludwig Maximilians University, Munich, ² Dept of Paediatrics, University of Essen, Essen, ³ Dept of Paediatric Pneumology and Allergology, Children's Hospital, University of Cologne, Cologne, and ⁴ Dept of Paediatric Pneumology and Immunology, Charité, Humboldt-University, Berlin, Germany.

CORRESPONDENCE: M. Griese, Children's Hospital, Ludwig Maximilians University, Lindwurmstr. 4, 80337 Munich, Germany. Fax: 49 8951607872. E-mail: matthias.griese{at}med.uni-muenchen.de

Keywords: Clara cell protein, cystic fibrosis, inflammation, lipoxin

Received: June 17, 2005
Accepted June 6, 2006

Lung inflammation plays a pivotal role in the pathogenesis of airway disease in cystic fibrosis (CF). An imbalance between pro- and anti-inflammatory mediators has been observed and a deficiency in the anti-inflammatory response has been proposed, but this concept remains controversial.

In the present study, the concentrations of two anti-inflammatory mediators, lipoxin A (LxA₄) and Clara cell protein 10 (CC-10), were assessed in bronchoalveolar lavage fluid (BALF) of CF patients with a wide range of endobronchial inflammation and disease controls with neutrophilic inflammation unrelated to CF.

No differences were observed in LxA₄ BALF concentrations between CF patients and controls with a similar degree of neutrophilic airway inflammation. Concentrations were also similar in CF patients with mild versus more severe airway inflammation. In contrast, CC-10 concentrations were lower in CF patients, but this decrease was limited to patients with more intense airway inflammation.

The present data do not support the concept of a primary defect in anti-inflammatory mediators in cystic fibrosis lung disease. Although Clara cell protein concentrations were found to be reduced, these alterations appear to be secondary to neutrophilic airway inflammation rather than due to a primary deficiency.

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