My research focuses on the relationship between peripheral inflammation and microglia. Lipopolysaccharide (LPS) is used to induce peripheral acute inflammation. It has been reported that LPS application induces microvesicle (MV) release from microglia in vitro, and these MVs contain inflammatory cytokines such as IL-1b. These data indicate that microglia detect peripheral inflammatory signals and react by releasing MVs. However, MVs released from microglia had not previously been observed in vivo. To observe microglial MVs, we made cranial windows into the heads of Iba1-GFP mice and performed in vivo live imaging using 2 photon-microscopy. GFP+ MVs were observed 24h after LPS injection (1 mg/kg, ip), and the peak of the increase in GFP+ MVs was at 48h after LPS injection. Because Iba1 is expressed in not only microglia but also some macrophages, we treated mice with clodronate (33 mg/kg, ip) to deplete peripheral macrophages. Clodronate treatment did not affect the increase of LPS-induced GFP+ MVs. This indicates that the GFP+ MVs were released from Iba1+ cells like microglia, but not macrophages. Interestingly, the GFP+ MVs were also observed in contact dermatitis model mice with chronic skin inflammation. These results provide a framework to study the role of microglial MVs in peripheral inflammatory mouse models.