Airway eosinophil accumulation and eotaxin-2/CCL24 expression following allergen challenge in BALB/c mice.

Eotaxin-1/CCL11 is important for early eosinophil recruitment to the airways of asthmatics. In order to clarify whether eotaxin-2/CCL24 accounts for prolonged airway eosinophilia, the authors determined the expression of CCL11 and CCL24 in lung tissue and bronchoalveolar lavage (BAL) as well as eosinophil infiltration over 14 days in BALB/c mice sensitised (intraperitonealy) and challenged (inhalations) with ovalbumin (OVA). Allergen exposure induced perivascular, peribronchial, and BAL eosinophilia for up to 7 days. CCL11 and CCL24 were highly expressed in lung tissue from 6 and up to 72 hours. Peak expression of CCL11 protein was 1557 +/- 109 pg/mL for OVA (mean +/- SEM) versus 404 +/- 73 pg/mL in controls (SAL) (P < .001) and 1690 +/- 54 versus 455 +/- 165 pg/mL for CCL24 (P < .01). In BAL, only eotaxin-2/CCL24 was significantly increased (1623 +/- 85 pg/mL for OVA versus 157 +/- 22 pg/mL for SAL, P < .01). Peak eosinophilia and CCL24 expression occurred later in BAL than in lung tissue. These data suggest that both CCL11 and CCL24 are important for recruitment of eosinophils to perivascular and peribronchial tissue seen up to 72 hours. This finding implies redundancy between these chemokines rather than differentially regulated expression over time. In contrast, only CCL24 seems important for recruitment of eosinophils into BAL. Specific inhibition of CCL11 alone is therefore unlikely to inhibit eosinophil recruitment to the airways.