Caspase-8 mediates inflammation and disease in rodent malaria.
Animals
Brain
/ pathology
Caspase 1
/ metabolism
Caspase 8
/ metabolism
Dendritic Cells
/ metabolism
Enzyme Activation
Extracellular Matrix
/ metabolism
Gene Expression Regulation
Humans
Inflammation
/ pathology
Interferon-gamma
/ metabolism
Interleukin-1beta
/ metabolism
Lipopolysaccharides
Malaria, Cerebral
/ enzymology
Mice, Inbred C57BL
Monocytes
/ metabolism
Plasmodium chabaudi
/ physiology
Spleen
/ metabolism
Toll-Like Receptors
/ metabolism
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
14 09 2020
14 09 2020
Historique:
received:
21
02
2019
accepted:
08
08
2020
entrez:
15
9
2020
pubmed:
16
9
2020
medline:
24
9
2020
Statut:
epublish
Résumé
Earlier studies indicate that either the canonical or non-canonical pathways of inflammasome activation have a limited role on malaria pathogenesis. Here, we report that caspase-8 is a central mediator of systemic inflammation, septic shock in the Plasmodium chabaudi-infected mice and the P. berghei-induced experimental cerebral malaria (ECM). Importantly, our results indicate that the combined deficiencies of caspases-8/1/11 or caspase-8/gasdermin-D (GSDM-D) renders mice impaired to produce both TNFα and IL-1β and highly resistant to lethality in these models, disclosing a complementary, but independent role of caspase-8 and caspases-1/11/GSDM-D in the pathogenesis of malaria. Further, we find that monocytes from malaria patients express active caspases-1, -4 and -8 suggesting that these inflammatory caspases may also play a role in the pathogenesis of human disease.
Identifiants
pubmed: 32929083
doi: 10.1038/s41467-020-18295-x
pii: 10.1038/s41467-020-18295-x
pmc: PMC7490701
doi:
Substances chimiques
Interleukin-1beta
0
Lipopolysaccharides
0
Toll-Like Receptors
0
Interferon-gamma
82115-62-6
Caspase 8
EC 3.4.22.-
Caspase 1
EC 3.4.22.36
Banques de données
figshare
['10.6084/m9.figshare.12751163.v1']
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
4596Subventions
Organisme : NIAID NIH HHS
ID : R01 AI079293
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI089681
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI150546
Pays : United States
Organisme : FIC NIH HHS
ID : R03 TW009007
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS098747
Pays : United States
Commentaires et corrections
Type : ErratumIn
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