TMEM173 Drives Lethal Coagulation in Sepsis.

Animals Bacterial Infections Blood Coagulation Calcium / metabolism Disease Models, Animal Humans Inflammasomes Intracellular Signaling Peptides and Proteins / metabolism Macrophages / metabolism Membrane Proteins / metabolism Mice Monocytes Phosphate-Binding Proteins / metabolism Pyroptosis Sepsis / metabolism Signal Transduction THP-1 Cells
ER stress GSDMD STING TMEM173 calcium coagulation inflammasome pyroptosis sepsis tissue factor

Journal

Cell host & microbe
ISSN: 1934-6069
Titre abrégé: Cell Host Microbe
Pays: United States
ID NLM: 101302316

Informations de publication

Date de publication:
08 04 2020
Historique:
received: 13 11 2019
revised: 14 01 2020
accepted: 10 02 2020
pubmed: 7 3 2020
medline: 30 12 2020
entrez: 7 3 2020
Statut: ppublish

Résumé

The discovery of TMEM173/STING-dependent innate immunity has recently provided guidance for the prevention and management of inflammatory disorders. Here, we show that myeloid TMEM173 occupies an essential role in regulating coagulation in bacterial infections through a mechanism independent of type I interferon response. Mechanistically, TMEM173 binding to ITPR1 controls calcium release from the endoplasmic reticulum in macrophages and monocytes. The TMEM173-dependent increase in cytosolic calcium drives Gasdermin D (GSDMD) cleavage and activation, which triggers the release of F3, the key initiator of blood coagulation. Genetic or pharmacological inhibition of the TMEM173-GSDMD-F3 pathway blocks systemic coagulation and improves animal survival in three models of sepsis (cecal ligation and puncture or bacteremia with Escherichia coli or Streptococcus pneumoniae infection). The upregulation of the TMEM173 pathway correlates with the severity of disseminated intravascular coagulation and mortality in patients with sepsis. Thus, TMEM173 is a key regulator of blood clotting during lethal bacterial infections.

Identifiants

DOI: 10.1016/j.chom.2020.02.004 PMID: 32142632 PMC: PMC7316085
pubmed: 32142632
pii: S1931-3128(20)30112-8
doi: 10.1016/j.chom.2020.02.004
pmc: PMC7316085
mid: NIHMS1599198
pii:
doi:

Substances chimiques

GSDMD protein, human 0
Gsdmd protein, mouse 0
Inflammasomes 0
Intracellular Signaling Peptides and Proteins 0
Membrane Proteins 0
Phosphate-Binding Proteins 0
STING1 protein, human 0
Sting1 protein, mouse 0
Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

556-570.e6

Subventions

Organisme : NCCIH NIH HHS
ID : R01 AT005076
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM063075
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM127027
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no conflicts of interest or financial interests.

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Auteurs

Hui Zhang (H)

Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.

Ling Zeng (L)

Wound Trauma Medical Center, State Key Laboratory of Trauma, Burns and Combined Injury, Daping Hospital, Army Medical University, Chongqing 400042, China.

Min Xie (M)

Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.

Jiao Liu (J)

The Third Affiliated Hospital, Protein Modification and Degradation Lab of Guangzhou and Guangdong, Guangzhou Medical University, Guang Zhou, Guangdong 510600, China.

Borong Zhou (B)

The Third Affiliated Hospital, Protein Modification and Degradation Lab of Guangzhou and Guangdong, Guangzhou Medical University, Guang Zhou, Guangdong 510600, China.

Runliu Wu (R)

Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Lizhi Cao (L)

Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.

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, Jiangsu 215163, China; Department of Women's and Children's Health, Karolinska University Hospital, 17176 Stockholm, Sweden.

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.

Herbert J Zeh (HJ)

Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Rui Kang (R)

Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA.

Jianxin Jiang (J)

Wound Trauma Medical Center, State Key Laboratory of Trauma, Burns and Combined Injury, Daping Hospital, Army Medical University, Chongqing 400042, China. Electronic address: jiangjx@cta.cq.cn.

Yan Yu (Y)

Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. Electronic address: xyyuyan@qq.com.

Daolin Tang (D)

The Third Affiliated Hospital, Protein Modification and Degradation Lab of Guangzhou and Guangdong, Guangzhou Medical University, Guang Zhou, Guangdong 510600, China; Department of Surgery, UT Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: daolin.tang@utsouthwestern.edu.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Infection › Infections bactériennes et mycoses › Infections bactériennes › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Phénomènes physiologiques respiratoires et circulatoires › Phénomènes physiogiques du sang › Hémostase › Coagulation sanguine › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Facteurs biologiques › Facteurs de la coagulation sanguine › Calcium › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Techniques d'investigation › Modèles théoriques › Modèles biologiques › Modèles animaux de maladie humaine › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Structures macromoléculaires › Complexes multiprotéiques › Inflammasomes › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Phagocytes › Macrophages › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Phagocytes › Monocytes › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines de transport › Protéines de liaison aux phosphates › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Mort cellulaire › Mort cellulaire régulée › Apoptose › Pyroptose › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › États, signes et symptômes pathologiques › Processus pathologiques › Inflammation › Sepsie › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › TMEM173 Drives Lethal Coagulation in Sepsis.
questionsmedicales.fr › Cellules › Cellules cultivées › Cellules cancéreuses en culture › Lignée cellulaire tumorale › Cellules THP-1 › TMEM173 Drives Lethal Coagulation in Sepsis.