A putative “chemokine switch” that regulates systemic acute inflammation in humans

Nabil Azhar, Rami A. Namas, Khalid Almahmoud, Akram Zaaqoq, Othman A. Malak, Derek Barclay, Jinling Yin, Fayten El-Dehaibi, Andrew Abboud, Richard L. Simmons, Ruben Zamora, Timothy R. Billiar, Yoram Vodovotz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


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.

Original languageEnglish
Article number9703
JournalScientific Reports
Issue number1
StatePublished - Dec 2021
Externally publishedYes


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