A putative "chemokine switch" that regulates systemic acute inflammation in humans.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
06 05 2021
06 05 2021
Historique:
received:
12
12
2020
accepted:
12
04
2021
entrez:
7
5
2021
pubmed:
8
5
2021
medline:
29
10
2021
Statut:
epublish
Résumé
Systemic inflammation is complex and likely drives clinical outcomes in critical illness such as that which ensues following severe injury. We obtained time course data on multiple inflammatory mediators in the blood of blunt trauma patients. Using dynamic network analyses, we inferred a novel control architecture for systemic inflammation: a three-way switch comprising the chemokines MCP-1/CCL2, MIG/CXCL9, and IP-10/CXCL10. To test this hypothesis, we created a logical model comprising this putative architecture. This model predicted key qualitative features of systemic inflammation in patient sub-groups, as well as the different patterns of hospital discharge of moderately vs. severely injured patients. Thus, a rational transition from data to data-driven models to mechanistic models suggests a novel, chemokine-based mechanism for control of acute inflammation in humans and points to the potential utility of this workflow in defining novel features in other complex diseases.
Identifiants
pubmed: 33958628
doi: 10.1038/s41598-021-88936-8
pii: 10.1038/s41598-021-88936-8
pmc: PMC8102583
doi:
Substances chimiques
Chemokines
0
Inflammation Mediators
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
9703Références
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