Increased serum concentration of G-CSF in cystic fibrosis patients with chronic Pseudomonas aeruginosa pneumonia

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BACKGROUND: Chronic Pseudomonas aeruginosa lung infection is the major reason for premature death in patients with cystic fibrosis (CF). Infected patients experience a progressive deterioration of the lung tissue caused by a persistent accumulation of PMNs. We investigated if the pulmonary accumulation of PMNs is reflected as a migration of PMNs through the blood in chronically infected CF patients.

METHODS: Blood and sputum samples from 37 stable, chronically (CF+P) and 6 non-infected (CF-P) CF patients without exacerbations were compared using FACS, leukocyte counting, and ELISA. Within the CF+P patients, the blood parameters were compared to the lung function (FEV1 and FVC) and to the sputum. Similar measurements were performed on 15 chronically infected CF patients before and after elective antibiotic treatment.

RESULTS: In the CF+P patients the concentration of G-CSF in the sera and PMNs in the blood was increased and correlated to poor lung function. However, only the concentration of G-CSF in the sera was correlated to the concentration of TNF-alpha in the sputum. After the antibiotic treatment, the lung function was improved and the concentration of PMNs in the blood and G-CSF in the sera was reduced.

CONCLUSION: G-CSF in the sera may contribute to the pulmonary inflammation in CF patients with chronic P. aeruginosa lung infection by regulating the number of PMNs available for migration and may be considered as an indicator of clinical status.

Original languageEnglish
JournalJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society
Issue number3
Pages (from-to)145-51
Number of pages7
Publication statusPublished - Aug 2006

    Research areas

  • Adolescent, Adult, Blood Cell Count, Cell Movement, Cystic Fibrosis, Female, Flow Cytometry, Granulocyte Colony-Stimulating Factor, Humans, Inflammation, Interleukin-8, Male, Middle Aged, Neutrophils, Pneumonia, Pseudomonas Infections, Tumor Necrosis Factor-alpha, Journal Article, Research Support, Non-U.S. Gov't

ID: 181873555