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Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

¹ Immunology Research Group, University of Saskatchewan, and the Divisions of, ² Respiratory Medicine and ³ Dermatology, Royal University Hospital, Saskatoon, SK, Canada

CORRESPONDENCE: J.R. Gordon, Dept of Veterinary Microbiology, 52 Campus Drive, University of Saskatchewan, Saskatoon, SK, Canada S7N 5B4. Fax: 1 3069667244. E-mail: john.gordon@usask.ca

Keywords: allergy, asthma, cytokines, eosinophils, salbutamol, sputum

Received: April 15, 2002
Accepted February 28, 2003

This work was supported by grants from the Saskatchewan Lung Association and the Canadian Institutes of Health Research.

Regular salbutamol use can exacerbate allergen-induced airway eosinophilia in asthmatics, but its effect on airway eosinophil chemokine responses is unknown.

Asthmatic subjects (n=14) were treated for 10 days with placebo or salbutamol in a double-blind, cross-over study, then given same-dose allergen challenges. Their sputa were then analysed 1 and 7 h later for a panel of eosinophil-related cytokines. Eosinophils from five test and three control subjects were tested for expression of CXCL8/interleukin (IL)-8, and its receptors and responsiveness to CCL11/eotaxin and CXCL8/IL-8.

Sputum CXCL8/IL-8, but not IL-5, CCL5/regulated on activation, T-cell expressed and secreted, CCL7/monocyte chemotactic protein-3, CCL11/eotaxin, granulocyte-macrophage colony-stimulating factor or tumour necrosis factor levels, were increased (42%) by the salbutamol treatments. The CXCL8/IL-8 levels correlated with the proportions of sputum eosinophils and these cells, but not other sputum cells, stained strongly for CXCL8/IL-8. The circulating eosinophils of the tested subjects (n=5) expressed CXCL8/IL-8 receptors and secreted high levels of this chemokine. Neutralisation of sputum CXCL8/IL-8 reduced eosinophil chemotactic responses to these samples by 19±5%.

These data suggest that regular use of salbutamol can augment airway CXCL8/interleukin-8 responses to allergen challenge and that this CXCL8/interleukin-8 could contribute to the airway inflammatory response.