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Alveolar macrophages and CC chemokines are increased in children with cystic fibrosis

¹ Telethon Institute for Child Health Research, ² Centre for Child Health Research, University of Western Australia, ³ Dept of Respiratory Medicine, Princess Margaret Hospital for Children, Perth, ⁴ School of Medicine, The University of Queensland, Brisbane, ⁵ Murdoch Children's Research Institute, Melbourne, Australia. ⁶ For details of the members of AREST CF, please see the Acknowledgements section.

CORRESPONDENCE: P. D. Sly, Division of Clinical Sciences, Telethon Institute for Child Health Research, P.O. Box 855, West Perth, WA 6872, Australia. E-mail: peters{at}ichr.uwa.edu.au

Keywords: CC chemokines, children, cystic fibrosis, macrophages

Received: November 24, 2008
Accepted April 6, 2009

Airway inflammation is an important component of cystic fibrosis (CF) lung disease. We sought to determine whether alveolar macrophages were involved in early CF lung disease.

Children with CF (median age 3.1 yrs) participated in a surveillance programme that included annual bronchoalveolar lavage (BAL). Control samples were obtained from non-CF children (median age 3.1 yrs; n = 24) investigated for persistent respiratory symptoms.

Pulmonary infection was detected in 31% (16 out of 51) and 38% (nine out of 24) of children from the CF and non-CF groups, respectively. Alveolar macrophages in BAL were increased in CF compared with non-CF in the absence of infection (223x10³ versus 85x10³ cells·mL^–1; p = 0.001) and were associated with elevations in the CC chemokines (macrophage inflammatory protein (MIP)-3 (chemokine (C-C motif) ligand (CCL)20; 355.8 versus 46.0 pg·mL^–1; p<0.001), monocyte chemotactic protein-1 (CCL2; 263.5 versus 25.3 pg·mL^–1; p<0.001), MIP-1 (CCL3; 38.2 versus 4.9 pg·mL^–1; p<0.001) and MIP-1β (CCL4; 326.6 versus 27.5 pg·mL^–1; p<0.001)). Total cell counts and neutrophil numbers increased in the presence of infection; however, there was no additional effect of CF.

Alveolar macrophages and CC chemokines are elevated in the lungs in young children with CF even in the absence of pulmonary infection. Longitudinal studies are required to determine the clinical relevance of these findings.