Sialylated proteins play an important role in leukocyte recruitment into inflamed tissue. This has been demonstrated recently using St3gal4 deficient mice where CXCR-2 mediated firm neutrophil arrest and extravasation were dramatically impaired (Frommhold et al., J.Exp.Med 2008). To address whether ST3Gal-IV has also a role on eosinophil trafficking, we investigated eosinophil recruitment into inflamed tissue in the absence of ST3Gal-IV. Eosinophil recruitment in St3gal4 deficient mice was examined using different models of eosinophilic inflammation in vivo: adhesion and extravasation of St3gal4 deficient eosinophils was significantly reduced in CCL11-induced inflammation of the cremaster muscle compared to control mice. In the 24 hour thioglycollate-induced peritonitis model, we found a marked reduction of eosinophil transmigration into the peritoneal cavity in the absence of ST3Gal-IV. In the ovalbumin induced asthma model, we found a significant reduction in eosinophil migration into the alveolar space in St3gal4-/-mice compared to control mice. Finally, eosinophil adhesion in flow chambers coated with E-selectin, VCAM-1, and CCL11 was significantly reduced in the absence of ST3Gal-IV.These findings show for the first time that ST3Gal-IV-dependent sialylation is crucial for eosinophil recruitment in vivo. Supported by Mizutani Grant Ref. Nr. 090063.