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Statins worse pulmonary fibrosis through enhancing NLRP3 inflammasome activation

Jin-Fu Xu, George R. Washko, Hui-Ping Li, Augustine M.K. Choi, Gary M. Hunninghake
European Respiratory Journal 2012 40: P2125; DOI:
Jin-Fu Xu
1Department of Pulmonary Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China
2Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States
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George R. Washko
2Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States
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Hui-Ping Li
1Department of Pulmonary Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China
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Augustine M.K. Choi
2Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States
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Gary M. Hunninghake
2Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States
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Abstract

The role of statins is controversial. To evaluate the association between statin use and ILD. We used regression analyses to evaluate the association between statin use and interstitial lung abnormalities (ILA) in a large cohort of smokers from COPDGene. Next, we evaluated the effect of statin pretreatment on bleomycin-induced fibrosis in mice and explored the mechanism behind these observations in vitro. In COPDGene, 38% of subjects with ILA were taking statins compared to 27% of subjects without ILA. Statin use was positively associated in ILA (odds ratio [OR] 1.60, 95% confidence interval [CI] 1.03-2.50, P=0.04) after adjustment for covariates including a history of high cholesterol or coronary artery disease. This association was modified by the hydrophilicity of statin and the age of the subject. Next, we demonstrate that statin administration aggravates lung injury and fibrosis in bleomycin-treated mice. Statin pretreatment enhances caspase-1-mediated immune responses in vivo and in vitro; the latter responses were abolished in bone marrow-derived macrophages (BMDM) isolated from Nlrp3-/- and Casp1-/- mice. Finally, we provide further insights by demonstrating that statins enhance NLRP3-inflammasome activation by increasing mitochondrial reactive oxygen species generation in macrophages. Statin use is associated with ILA among smokers in the COPDGene study and enhances bleomycin-induced lung inflammation and fibrosis in the mouse through a mechanism involving enhanced NLRP3-inflammasome activation. Our findings suggest that clinicians should be aware that radiological evidence of ILD can develop in some COPD patients treated with statins.

  • COPD - management
  • Immunology
  • Lung injury
  • © 2012 ERS
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Statins worse pulmonary fibrosis through enhancing NLRP3 inflammasome activation
Jin-Fu Xu, George R. Washko, Hui-Ping Li, Augustine M.K. Choi, Gary M. Hunninghake
European Respiratory Journal Sep 2012, 40 (Suppl 56) P2125;

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Statins worse pulmonary fibrosis through enhancing NLRP3 inflammasome activation
Jin-Fu Xu, George R. Washko, Hui-Ping Li, Augustine M.K. Choi, Gary M. Hunninghake
European Respiratory Journal Sep 2012, 40 (Suppl 56) P2125;
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