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10.1073/pnas.2202012119

http://scihub22266oqcxt.onion/10.1073/pnas.2202012119
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suck abstract from ncbi


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pmid35588457      Proc+Natl+Acad+Sci+U+S+A 2022 ; 119 (21): e2202012119
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  • Caspase-4/11 exacerbates disease severity in SARS-CoV-2 infection by promoting inflammation and immunothrombosis #MMPMID35588457
  • Eltobgy MM; Zani A; Kenney AD; Estfanous S; Kim E; Badr A; Carafice C; Daily K; Whitham O; Pietrzak M; Webb A; Kawahara J; Eddy AC; Denz P; Lu M; Kc M; Peeples ME; Li J; Zhu J; Que J; Robinson R; Rosas Mejia O; Rayner RE; Hall-Stoodley L; Seveau S; Gavrilin MA; Zhang X; Thomas J; Kohlmeier JE; Suthar MS; Oltz E; Tedeschi A; Robledo-Avila FH; Partida-Sanchez S; Hemann EA; Abdelrazik E; Forero A; Nimjee SM; Boyaka PN; Cormet-Boyaka E; Yount JS; Amer AO
  • Proc Natl Acad Sci U S A 2022[May]; 119 (21): e2202012119 PMID35588457show ga
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a worldwide health concern, and new treatment strategies are needed. Targeting inflammatory innate immunity pathways holds therapeutic promise, but effective molecular targets remain elusive. Here, we show that human caspase-4 (CASP4) and its mouse homolog, caspase-11 (CASP11), are up-regulated in SARS-CoV-2 infections and that CASP4 expression correlates with severity of SARS-CoV-2 infection in humans. SARS-CoV-2-infected Casp11-/- mice were protected from severe weight loss and lung pathology, including blood vessel damage, compared to wild-type (WT) mice and mice lacking the caspase downstream effector gasdermin-D (Gsdmd-/-). Notably, viral titers were similar regardless of CASP11 knockout. Global transcriptomics of SARS-CoV-2-infected WT, Casp11-/-, and Gsdmd-/- lungs identified restrained expression of inflammatory molecules and altered neutrophil gene signatures in Casp11-/- mice. We confirmed that protein levels of inflammatory mediators interleukin (IL)-1beta, IL-6, and CXCL1, as well as neutrophil functions, were reduced in Casp11-/- lungs. Additionally, Casp11-/- lungs accumulated less von Willebrand factor, a marker for endothelial damage, but expressed more Kruppel-Like Factor 2, a transcription factor that maintains vascular integrity. Overall, our results demonstrate that CASP4/11 promotes detrimental SARS-CoV-2-induced inflammation and coagulopathy, largely independently of GSDMD, identifying CASP4/11 as a promising drug target for treatment and prevention of severe COVID-19.
  • |*COVID-19/enzymology/pathology[MESH]
  • |*SARS-CoV-2[MESH]
  • |*Thromboinflammation/enzymology/genetics[MESH]
  • |Animals[MESH]
  • |Caspases, Initiator/genetics/*metabolism[MESH]
  • |Disease Progression[MESH]
  • |Humans[MESH]
  • |Lung/pathology[MESH]
  • |Mice[MESH]
  • |Mice, Knockout[MESH]


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