@article {YatomiP532, author = {Masakiyo Yatomi and Takeshi Hisada and Masaki Nishioka and Yosuke Kamide and Hiroaki Tsurumaki and Haruka Aoki and Kaori Seki and Reiko Yoshino and Akihiro Ono and Yasuhiko Koga and Kunio Dobashi and Tamotsu Ishizuka and Masatomo Mori}, title = {17(R)-resolvin D1 attenuates bleomycin-induced lung fibrosis in mice}, volume = {42}, number = {Suppl 57}, elocation-id = {P532}, year = {2013}, publisher = {European Respiratory Society}, abstract = {Idiopathic pulmonary fibrosis(IPF) is a destructive inflammatory disease leading to pulmonary fibrosis with limited therapeutic options. Neutrophilic inflammation plays a pivotal role in IPF. Resolvins are a family of potent lipid mediators and promote the resolution of the imflammatory response back to a non-inflamed state.17(R)-resolvin D1(17(R)-RvD1) is an aspirin-triggered epimer of resolvin D1 derived from docosahexaenoic acid and resists rapid inactivation by eicosanoid oxidoreductases. Bleomycin(BLM) is a well-established agent for inducing pulmonary inflammation and fibross. We examined anti-inflammatory and anti-fibrotic effects of 17(R)-RvD1 on lung fibrosis in BLM-treated mice.We chose continuous subctaneous administration of BLM for 1week to 8-to-10-wk-old female C57BL/6 mice. 17(R)-RvD1 was injected intraperitoneally for five days consecutively.Fourteen days after BLM treatment, 17(R)-RvD1 reduced neutophilia in bronchoaveolar fluid(BAL) and decreased gene expression of IL-1β, inflammatory cytokines,in the lung tissue compared with control mice. Twenty-eight days after BLM exposure, 17(R)-RvD1 attenuated BLM induced pulmonary fibrosis histologically and decreased hydroxyproline content. Connective tissue growth factor(CTGF) is a cysteine-rich mitogenic peptide that is implicated in various fibrotic disorders and induced in fibroblasts after activation with transforming growth factor-β (TGF-β). At 28th day, decreased gene expression of CTGF in 17(R)-RvD1-treated mice was observed. These results suggest that 17(R)-RvD1 attenuates pulmonary fibrosis through the promotion of resolution in neutrophilic inflammation.}, issn = {0903-1936}, URL = {https://erj.ersjournals.com/content/42/Suppl_57/P532}, eprint = {https://erj.ersjournals.com/content/42/Suppl_57/P532.full.pdf}, journal = {European Respiratory Journal} }