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More specifically speaking, the mechanism potentially involved downregulation of macrophage CD11b, which played a vital role in monocyte adhesion, as well as decreased expression of macrophage modulators including CXCL-10, CXCL-1, C-C motif chemokine ligand-1 (CCL-2) and tissue inhibitor of metal protease-1 (TIMP-1) (Robinson et al., 2015)