These findings, together with previous studies demonstrating decreased eosinophilia in allergen-challenged Gal-3-/- mice (Zuberi et al., 2004; Ge et al., 2010) suggest that endogenous Gal-3, whether extracellular (as soluble protein in BALF) or intracellular (contained within or bound to surface glycan ligands of certain cell types in lung tissue), is critically involved in Eos recruitment to the airways of acute and chronic allergen-challenged mice. Here, LGALS3 is linked to Increased total eosinophil count.