Antiviral and Anti-Inflammatory Activities of Pochonin D, a Heat Shock Protein 90 Inhibitor, against Rhinovirus Infection

Song, Jae-Hyoung; Shim, Aeri; Kim, Yeon-Jeong; Ahn, Jae-Hee; Kwon, Bo-Eun; Pham, Thuy Trang; Lee, Jongkook; Chang, Sun-Young; Ko, Hyun-Jeong

Recent studies suggest that myeloid-derived suppressor cells (MDSCs), which expand during cancer, inflammation, and infection, might be involved in increasing the level of cytokines and chemokines in influenza-induced pulmonary inflammation (Jeisy-Scott et al., 2011; Atretkhany and Drutskaya, 2016) . We investigated whether the same was true for rhinovirus. We therefore assessed cellular infiltration of neutrophils into the BALF of HRV1B-infected mice treated with pochonin D or vehicle (Fig. 4) . CD11c + F4/80 + alveolar macrophages were excluded from the gating for neutrophils. The number of MDSCs in BALF showing the phenotype of granulocytic neutrophils was significantly higher in rhinovirus-infected mice than in non-infected mice. Moreover, the number of these cells decreased with pochonin D treatment in virus-infected mice (Fig. 4B) . Similarly, the percentage of MDSC cells in BALF from rhinovirus-infected mice was higher than that in control mice, and the percentage of granulocytic neutrophils in BALF from HRV1B-infected mice was reduced by pochonin D treatment. Thus, we could confirm that inflammatory cell infiltrates in the lung were significantly increased by HRV1B infection, and could be significantly inhibited by administration of pochonin D.