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Interferon-ß alleviates sepsis by SIRT1-mediated blockage of endothelial glycocalyx shedding.
Duan, Suhong; Kim, Seung-Gook; Lim, Hyung-Jin; Song, Hwa-Ryung; Han, Myung-Kwan.
Afiliação
  • Duan S; Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
  • Kim SG; Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
  • Lim HJ; Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
  • Song HR; Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
  • Han MK; Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896, Korea.
BMB Rep ; 56(5): 314-319, 2023 May.
Article em En | MEDLINE | ID: mdl-37013347
Sepsis is a life-threatening multi-organ dysfunction with high mortality caused by the body's improper response to microbial infection. No new effective therapy has emerged that can adequately treat patients with sepsis. We previously demonstrated that interferon-ß (IFN-ß) protects against sepsis via sirtuin 1-(SIRT1)-mediated immunosuppression. Another study also reported its significant protective effect against acute respiratory distress syndrome, a complication of severe sepsis, in human patients. However, the IFN-ß effect cannot solely be explained by SIRT1-mediated immunosuppression, since sepsis induces immunosuppression in patients. Here, we show that IFN-ß, in combination with nicotinamide riboside (NR), alleviates sepsis by blocking endothelial damage via SIRT1 activation. IFN-ß plus NR protected against cecal ligation puncture-(CLP)-induced sepsis in wild-type mice, but not in endothelial cell-specific Sirt1 knockout (EC-Sirt1 KO) mice. IFN-ß upregulated SIRT1 protein expression in endothelial cells in a protein synthesisindependent manner. IFN-ß plus NR reduced the CLP-induced increase in in vivo endothelial permeability in wild-type, but not EC-Sirt1 KO mice. IFN-ß plus NR suppressed lipopolysaccharide-induced up-regulation of heparinase 1, but the effect was abolished by Sirt1 knockdown in endothelial cells. Our results suggest that IFN-ß plus NR protects against endothelial damage during sepsis via activation of the SIRT1/heparinase 1 pathway. [BMB Reports 2023; 56(5): 314-319].
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sepse / Sirtuína 1 Limite: Animals / Humans Idioma: En Revista: BMB Rep Assunto da revista: BIOLOGIA MOLECULAR / BIOQUIMICA Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sepse / Sirtuína 1 Limite: Animals / Humans Idioma: En Revista: BMB Rep Assunto da revista: BIOLOGIA MOLECULAR / BIOQUIMICA Ano de publicação: 2023 Tipo de documento: Article