Mechanisms of allergen- and LPS-induced bone marrow eosinophil mobilization and eosinophil accumulation into the pleural cavity: a role for CD11b/CD18 complex

Objective: The mechanisms involved in bone marrow eosinophil emigration and recruitment to inflammatory sites are not fully understood. The involvemen t of CD11b/CD18 in marrow eosinophil release induced by lipopolysaccharide (LPS) or allergen was investigated in mice. Methods: Eosinophil and neutrophil counts in the pleural cavity, blood and bone marrow were performed at different time intervals after the intrathora cic injection of LPS (250 ng/ cavity) or ovalbumin (OVA, 12 mug/cavity; int o actively sensitized mice) and compared to anti-CD11b/CD18 (5C6, 1 mg/mous e) or anti-IL-5 (TRFK-5, 500 mug/kg) treated mice. Results. LPS induced local eosinophil influx, that peaked within 24 h and t hat was preceded by a decrease in marrow eosinophils at 4 h. Antigenic chal lenge induced a decrease in marrow eosinophils within 4 h, followed by a lo ng lasting pleural eosinophil accumulation and a persistent increase in mar row eosinophil numbers. Pretreatment with anti-CD11b/CD18 abolished LPS-ind uced neutrophil and eosinophil accumulation in the pleural cavity at 4 and 24 h, respectively. This pretreatment failed to modify neutrophil emigratio n from bone marrow, but significantly inhibited marrow eosinophil release a t 4 h post-LPS or OVA challenge. Anti-IL-5 pretreatment failed to inhibit L PS-induced pleural eosinophil accumulation and mobilization from bone marro w, but it abolished allergen-induced effects, indicating a role for IL-5 in marrow eosinophil mobilization induced by antigen, but not by LPS challeng e. Conclusions: Our results suggest that eosinophil migration induced by antig en or LPS into the pleural cavity is preceded by bone marrow eosinophil rel ease through a mechanism that depends on CD11b/CD18.