Eotaxin-2 and eotaxin-3 expression is associated with persistent eosinophilic bronchial inflammation in patients with asthma after allergen challenge - 18/08/11
, Fabio L.M. Ricciardolo, MD, PhD a, b, Annemarie van Schadewijk, MSc a, Klaus F. Rabe, MD, PhD a, Peter J. Sterk, MD, PhD a, Pieter S. Hiemstra, PhD a, Thais Mauad, MD, PhD a, c
Reprint requests: A. Janneke Ravensberg, MD, Leiden University Medical Center, Lung Function Laboratory C2-P-62, PO Box 9600, 2300 RC Leiden, The Netherlands.Leiden, The Netherlands, Genoa, Italy, and São Paulo, Brazil
Abstract |
Background |
Eotaxin-1, eotaxin-2, and eotaxin-3 are chemokines involved in the activation and recruitment of eosinophils through activation of their main receptor, CC chemokine receptor 3. The differential roles of these chemokines still remain to be established. It has been suggested that eotaxin-1 is an important mediator in the early phase of allergen-induced recruitment of eosinophils into the airways. Eotaxin-2 and eotaxin-3 might play a role in the subsequent persistence of allergen-induced bronchial eosinophilia.
Objective |
The aim of this study was to determine the expression of eotaxins and eosinophil counts in the bronchial mucosa of subjects with mild asthma after resolution of the late-phase asthmatic response (LAR).
Methods |
The expression of eotaxins and eosinophil counts were determined in bronchial biopsy specimens obtained from 10 subjects with mild asthma 48 hours after diluent and allergen challenge by using immunohistochemistry. Positively stained cells were counted in a 125-μm-deep zone of the lamina propria.
Results |
Eotaxin-2 and eotaxin-3 expression in bronchial mucosa was significantly increased 48 hours after allergen challenge (P=.001 and P=.013, respectively). At this time point, when marked tissue eosinophilia was still present, these increases were positively correlated with the magnitude of the LAR (r=0.72, P=.019 and r=0.64, P=.046, respectively). Furthermore, eotaxin-2 expression was associated with the number of eosinophils after allergen challenge (r=0.72, P=.018).
Conclusion |
Our findings suggest that eotaxin-2 and eotaxin-3 might account for the persistence of bronchial eosinophilia after resolution of the LAR.
El texto completo de este artículo está disponible en PDF.Key words : Asthma, allergen, eotaxin-1 (CCL11), eotaxin-2 (CCL24), eotaxin-3 (CCL26), eosinophil, chemokines, bronchial biopsy, airways inflammation
Abbreviations used : CCR3, EAR, LAR
Esquema
| Supported by a research grant from GlaxoSmithKline. Disclosure of potential conflict of interest: A. J. Ravensberg—none disclosed. F. L. M. Ricciardolo—none disclosed. A. van Schadewijk—none disclosed. K. F. Rabe has consulting agreements with, has participated in advisory board meetings of, and received lecture fees from AstraZeneca, Boehringer, Pfizer, Novartis, AltanaPharma, MSD, and GSK. The Department of Pulmonology and thus Professor Rabe, as head of the department, has received grants from AltanaPharma, Novartis, Bayer, AstraZeneca, Pfizer, MSD, Exhale Therapeutics, and GSK in the years 2001-2004. P. J. Sterk—none disclosed. P. S. Hiemstra—none disclosed. T. Mauad—none disclosed. |
Vol 115 - N° 4
P. 779-785 - avril 2005 Regresar al número
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