Taxanes frequently cause chemotherapy-induced peripheral neuropathy (CIPN). However, the mechanisms underlying CIPN pathogenesis are not fully understood. We previously showed that taxanes preferentially impair Schwann cells (SCs) by inducing dedifferentiation. In this study, we further examined the roles of dedifferentiated SCs in the development of CIPN. We found that mRNA expression of an inflammatory factor, X, was increased in dedifferentiated SC culture or the mouse sciatic nerve after paclitaxel (0.01 μM) treatment or repeated i.p. injection of paclitaxel (20 mg/kg), respectively. Furthermore, murine macrophage cell line (RAW264.7) showed a chemotaxis response toward the conditioned medium of paclitaxel-treated SCs. Consistent with this, we found that the perineural application of an inflammatory factor derived from dedifferentiated SCs induced infiltration of macrophages into the sciatic nerve and mechanical hypersensitivity in mice. Taken together, our findings allow us to conclude that, in response to paclitaxel treatment, an inflammatory factor is released from dedifferentiated SCs to chemoattract macrophages. These SC-dependent macrophage migration may participate in paclitaxel-induced CIPN pathogenesis.