Can hypertonic saline inhalation influence preformed chemokine and mediator release in induced sputum of chronic obstructive pulmonary disease patients? Comparison with isotonic saline
Article first published online: 17 OCT 2007
Clinical & Experimental Allergy
Volume 37, Issue 12, pages 1819–1826, December 2007
How to Cite
Cianchetti, S., Bacci, E., Bartoli, M. L., Ruocco, L., Pavia, T., Dente, F. L., Di Franco, A., Vagaggini, B. and Paggiaro, P. (2007), Can hypertonic saline inhalation influence preformed chemokine and mediator release in induced sputum of chronic obstructive pulmonary disease patients? Comparison with isotonic saline. Clinical & Experimental Allergy, 37: 1819–1826. doi: 10.1111/j.1365-2222.2007.02850.x
- Issue published online: 17 OCT 2007
- Article first published online: 17 OCT 2007
- Submitted 21 February 2007; revised 5 September 2007; accepted 7 September 2007
- induced sputum
Background Hypertonic saline (HS) has been shown to modulate in vitro cell functions according to the state of cell activation; however, few studies have evaluated the effect of HS in vivo. Chronic airway inflammation, a major feature of chronic obstructive pulmonary disease (COPD), is associated with an activation of inflammatory and resident cells, which in turn makes them more prompt to respond to further stimuli.
Objective To evaluate whether HS might modulate, also in vivo, the release of preformed mediators and intracellular chemokines from airway cells of COPD patients.
Methods Sputum was induced by inhalation of either HS (4.5% w/v) or isotonic saline (IS 0.9% w/v) solution and processed by plug selection. We measured eosinophil cationic protein (ECP), neutrophil elastase (NE), IL-8 and monocyte chemoattractant protein-1 (MCP-1) in sputum samples obtained by either HS or IS inhalation in 24 COPD patients.
Results No significant difference in mediators measured in sputum samples obtained by the two different inductions was observed; also, there was no significant difference in sputum sample volumes, cell viability, total and differential cell counts. Repeatability between the two tests was high for ECP, NE, macrophages, neutrophils and eosinophils, and satisfactory for IL-8 and MCP-1.
Conclusions Hyperosmolarity does not affect the levels of the inflammatory mediators and chemokines examined or the cell counts measured in induced sputum obtained from COPD patients. This study does not support the hypothesis that HS can stimulate chemokine and mediator release from airway cells of COPD patients. Therefore, HS and IS can be interchangeably used to measure inflammatory mediators in the sputum supernatant of COPD patients.