The effect of treatment of cystic fibrosis pulmonary exacerbations on airways and systemic inflammation.
BACKGROUND
Chronic infection in cystic fibrosis (CF) and airway inflammation leads to progressive lung injury. Neutrophils are considered to be responsible for the onset and promotion of the inflammatory response within the CF lung. The relationship between infection and inflammation is complex but circulating inflammatory markers may not truly reflect the local inflammatory response in the lung. The aims of this study were to investigate the change of inflammatory biomarkers and cells within sputum and blood before and after intravenous antibiotics for a pulmonary exacerbation of CF.


METHODS
Assays included neutrophil elastase (NE) and complex, interleukin-8 (IL-8) and soluble intercellular adhesion molecule-1 (sICAM-1), fas ligand (FAS-L), and TNFr-1. Analysis of sputum cell differential and absolute cell counts and immunocytochemistry (CD11b and CD95) on sputum and isolated blood neutrophils were carried out.


RESULTS
There were no significant differences in absolute or differential sputum cell counts or sputum sol measurements following antibiotics. There was a significant increase in the percentage of blood neutrophils with minimal CD11b staining, 28 (4.1) mean percentage (SEM) versus 41 (2.9) and a decrease in the percentage showing maximal staining 30 (0.5) versus 15 (2.5). There was a significant increase in the percentage of blood neutrophils without CD95 staining, 43 (5.4) mean percentage versus 52 (5.1).


CONCLUSIONS
These data suggest a modifiable systemic response to i.v. antibiotics but a local sustained inflammatory response in the lung.
Downey
Damian G
DG
Respiratory Research Group, Queens University of Belfast, Belfast, Northern Ireland, UK.
Brockbank
Simon
S
Martin
S Lorraine
SL
Ennis
Madeleine
M
Elborn
J Stuart
JS
D000293:Adolescent; D000328:Adult; D000900:Anti-Bacterial Agents / Q000008:administration & dosage / Q000627:therapeutic use; D015415:Biomarkers / Q000032:analysis*; D039481:CD11b Antigen / Q000032:analysis*; D002470:Cell Survival; D003550:Cystic Fibrosis / Q000188:drug therapy*; D053222:Fas Ligand Protein / Q000032:analysis; D006651:Histocytochemistry; D006801:Humans; D007275:Injections, Intravenous; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D007958:Leukocyte Count; D008171:Lung Diseases / Q000188:drug therapy*; D009504:Neutrophils / Q000737:chemistry* / Q000473:pathology; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000032:analysis; D013183:Sputum / Q000166:cytology*; D019014:fas Receptor / Q000032:analysis*
D000900:Anti-Bacterial Agents; D015415:Biomarkers; D039481:CD11b Antigen; D053222:Fas Ligand Protein; D016209:Interleukin-8; D047888:Receptors, Tumor Necrosis Factor, Type I; D019014:fas Receptor; D018799:Intercellular Adhesion Molecule-1