“…In addition, numerous reports have demonstrated that the infiltration of circulating leukocytes (i.e., monocytes/macrophages and neutrophils) to the damaged nervous system contributes significantly to chronic neuroinflammation (Liu et al, 2000;Hu and McLachlan, 2002;Thacker et al, 2007; Austin and Moalem-Taylor, 2010;Calvo et al, 2012). Particularly, macrophages account for the largest population among infiltrating leukocytes in injured peripheral nerves, and the depletion of macrophages clearly prevents experimental neuropathic pain in rodents (Liu et al, 2000;Mert et al, 2009;Kobayashi et al, 2015). Moreover, it has been reported that several inflammatory cytokines [e.g., interleukin (IL)-1b and tumor necrosis factor a (TNFa)] and chemokines [e.g., CC-chemokine ligand (CCL) 3 and CCL4], derived from inflammatory macrophages, exert functions as key neuroinflammatory regulators that directly enhance the excitability of primary sensory neurons and prolong neuroinflammation, facilitating neuropathic pain (Sommer and Kress, 2004;Scholz and Woolf, 2007;Lee and Zhang, 2012;Saika et al, 2012).…”