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-mum-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.

Eotaxin-2 and eotaxin-3 expression is associated with persistent eosinophilic bronchial inflammation in patients with asthma after allergen challenge

RICCIARDOLO, Fabio Luigi Massimo;
2005

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-mum-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.
115
779
785
RAVENSBERG AJ; RICCIARDOLO FLM; VAN SCHADEWIJK A; RABE KF; STERK PJ; HIEMSTRA PS; MAUAD T
File in questo prodotto:
File Dimensione Formato  
Ravensberg JACI2005.pdf

Accesso riservato

Tipo di file: POSTPRINT (VERSIONE FINALE DELL’AUTORE)
Dimensione 963.88 kB
Formato Adobe PDF
963.88 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2318/40377
Citazioni
  • ???jsp.display-item.citation.pmc??? 37
  • Scopus 80
  • ???jsp.display-item.citation.isi??? 76
social impact