Surfactant proteins SP-B and SP-C and their precursors in bronchoalveolar lavages from children with acute and chronic inflammatory airway disease

被引:22
|
作者
Tafel O. [1 ]
Latzin P. [1 ,2 ]
Paul K. [3 ]
Winter T. [1 ]
Woischnik M. [1 ]
Griese M. [1 ]
机构
[1] Lung Research Group, Children's Hospital, Ludwig Maximilian University, Munich
[2] Division of Respiratory Medicine, Department of Paediatrics, Inselspital and University of Bern, Bern
[3] Praxis Karl Paul, Berlin
关键词
Cystic Fibrosis; Chronic Bronchitis; Surfactant Protein; Alveolar Space; Primary Ciliary Dyskinesia;
D O I
10.1186/1471-2466-8-6
中图分类号
学科分类号
摘要
Background: The surfactant proteins B (SP-B) and C (SP-C) are important for the stability and function of the alveolar surfactant film. Their involvement and down-regulation in inflammatory processes has recently been proposed, but their level during neutrophilic human airway diseases are not yet known. Methods: We used 1D-electrophoresis and Western blotting to determine the concentrations and molecular forms of SP-B and SP-C in bronchoalveolar lavage (BAL) fluid of children with different inflammatory airway diseases. 21 children with cystic fibrosis, 15 with chronic bronchitis and 14 with pneumonia were included and compared to 14 healthy control children. Results: SP-B was detected in BAL of all 64 patients, whereas SP-C was found in BAL of all but 3 children; those three BAL fluids had more than 80% neutrophils, and in two patients, who were re-lavaged later, SP-C was then present and the neutrophil count was lower. SP-B was mainly present as a dimer, SP-C as a monomer. For both qualitative and quantitative measures of SP-C and SP-B, no significant differences were observed between the four evaluated patient groups. Conclusion: Concentration or molecular form of SP-B and SP-C is not altered in BAL of children with different acute and chronic inflammatory lung diseases. We conclude that there is no down-regulation of SP-B and SP-C at the protein level in inflammatory processes of neutrophilic airway disease. © 2008 Tafel et al; licensee BioMed Central Ltd.
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