Research has indicated that CCL11 operates through a myeloid cell-specific nuclear factor-kappa B-dependent pathway in experimental colitis.[44] Bone marrow chimera experiments revealed that Ly6C(high)CCR2(+) inflammatory monocytes/macrophages mediate CCL11-driven mechanisms,[44] with F4/80(+)CD11b(+)CCR2(+)Ly6C(high) monocytes expressing CCL11, whose recruitment correlates positively with colonic eosinophilic inflammation. This evidence concerns the gene CCR2 and colitis.