Emerging mechanisms of immunocoagulation in sepsis and septic shock.


Journal

Trends in immunology
ISSN: 1471-4981
Titre abrégé: Trends Immunol
Pays: England
ID NLM: 100966032

Informations de publication

Date de publication:
06 2021
Historique:
received: 26 12 2020
revised: 31 03 2021
accepted: 01 04 2021
pubmed: 29 4 2021
medline: 6 7 2021
entrez: 28 4 2021
Statut: ppublish

Résumé

Sepsis and septic shock driven by microbial infections are still among the most challenging health problems, causing 11 million deaths worldwide every year. How does the host's response to pathogen infections effectively restore homeostasis instead of precipitating pathogenic and potentially fatal feedforward reactions? Recently, there have been significant new advances in our understanding of the interface between mammalian immunity and coagulation ('immunocoagulation') and its impact on sepsis. In particular, the release and activation of F3 (the main initiator of coagulation) from and on myeloid or epithelial cells is facilitated by activating inflammasomes and consequent gasdermin D (GSDMD)-mediated pyroptosis, coupled to signaling via high mobility group box 1 (HMGB1), stimulator of interferon response CGAMP interactor 1 (STING1), or sequestosome 1 (SQSTM1). Pharmacological modulation of the immunocoagulation pathways emerge as novel and potential therapeutic strategies for sepsis.

Identifiants

pubmed: 33906793
pii: S1471-4906(21)00072-7
doi: 10.1016/j.it.2021.04.001
pmc: PMC8436187
mid: NIHMS1737551
pii:
doi:

Substances chimiques

Intracellular Signaling Peptides and Proteins 0
Phosphate-Binding Proteins 0
Caspases, Initiator EC 3.4.22.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

508-522

Subventions

Organisme : NIGMS NIH HHS
ID : R01 GM127791
Pays : United States

Informations de copyright

Copyright © 2021 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests No conflicts of interest to declare.

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Auteurs

Daolin Tang (D)

The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120, China; Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: daolin.tang@utsouthwestern.edu.

Haichao Wang (H)

Laboratory of Emergency Medicine, North Shore University Hospital and the Feinstein Institute for Medical Research, Manhasset, NY 11030, USA.

Timothy R Billiar (TR)

Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15219, USA.

Guido Kroemer (G)

Equipe Labellisée par la Ligue Contre le Cancer, Université de Paris, Sorbonne Université, INSERM U1138, Centre de Recherche des Cordeliers, Paris, France; Metabolomics and Cell Biology Platforms, Gustave Roussy Cancer Campus; 94800 Villejuif, France; Pôle de Biologie, Hôpital Européen Georges Pompidou, AP-, HP; 75015 Paris, France; Suzhou Institute for Systems Medicine, Chinese Academy of Sciences, Suzhou, China; Department of Women's and Children's Health, Karolinska University Hospital, 17176 Stockholm, Sweden.

Rui Kang (R)

Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: rui.kang@utsouthwestern.edu.

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