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Am. J. Respir. Crit. Care Med., Volume 156, Number 4, October 1997, 1197-1204

Lower Airway Inflammation in Infants and Young Children with Cystic Fibrosis

DAVID S. ARMSTRONG, KEITH GRIMWOOD, JOHN B. CARLIN, ROSEMARY CARZINO, JOSE P. GUTIÈRREZ, JEREMY HULL, ANTHONY OLINSKY, ETHNA M. PHELAN, COLIN F. ROBERTSON, and PETER D. PHELAN

Departments of Thoracic Medicine and Radiology, Royal Children's Hospital and Clinical Epidemiology and Biostatistics Unit; Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia

Airway inflammation is an important component of cystic fibrosis (CF) lung disease. To determine whether this begins early in the illness, before the onset of infection, we examined bronchoalveolar lavage (BAL) fluid from 46 newly diagnosed infants with CF under the age of 6 mo identified by a neonatal screening program. These infants were divided into three groups: 10 had not experienced respiratory symptoms or received antibiotics and pathogens were absent in their BAL fluid; 18 had clear evidence of lower respiratory viral or bacterial (>=  105 CFU/ml) infection; and the remaining 18 had either respiratory symptoms, taken antibiotics, or had < 105 CFU/ml of respiratory pathogens. Their BAL cytology, interleukin-8, and elastolytic activity were compared with those from 13 control subjects. In a longitudinal study to assess if inflammation develops or persists in the absence of infection, the results of 56 paired annual BAL specimens from 44 CF infants were grouped according to whether they showed absence, development, clearance, or persistence of infection. In newly diagnosed infants with CF, those without infection had BAL profiles comparable with control subjects while those with a lower respiratory infection had evidence of airway inflammation. In older children, the development and persistence of infection was accompanied by increased inflammatory markers, whereas these were decreased in the absence, or with the clearance, of infection. We conclude that airway inflammation follows respiratory infection and, in young children, improves when pathogens are eradicated from the airways.




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L. C. Lands, V. Grey, A. A. Smountas, V. G. Kramer, and D. McKenna
Lymphocyte Glutathione Levels in Children With Cystic Fibrosis
Chest, July 1, 1999; 116(1): 201 - 205.
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 Am. J. Respir. Crit. Care Med.Home page
M. S. MUHLEBACH, P. W. STEWART, M. W. LEIGH, and T. L. NOAH
Quantitation of Inflammatory Responses to Bacteria in Young Cystic Fibrosis and Control Patients
Am. J. Respir. Crit. Care Med., July 1, 1999; 160(1): 186 - 191.
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 Am. J. Physiol. Cell Physiol.Home page
L. M. Schwiebert, K. Estell, and S. M. Propst
Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression
Am J Physiol Cell Physiol, March 1, 1999; 276(3): C700 - C710.
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 Physiol. Rev.Home page
J. M. PILEWSKI and R. A. FRIZZELL
Role of CFTR in Airway Disease
Physiol Rev, January 1, 1999; 79(1): 215 - 255.
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 Am. J. Respir. Cell Mol. Bio.Home page
H. R. Black, J. R. Yankaskas, L. G. Johnson, and T. L. Noah
Interleukin-8 Production by Cystic Fibrosis Nasal Epithelial Cells after Tumor Necrosis Factor-alpha and Respiratory Syncytial Virus Stimulation
Am. J. Respir. Cell Mol. Biol., August 1, 1998; 19(2): 210 - 215.
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