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The Use of Mouse Splenocytes to Assess Pathogen-associated Molecular Pattern Influence on Clock Gene Expression
Published on: July 24, 2018
Circadian Disruption Exacerbates Innate Immune Responses by Modulating the Bistability of Pro-Inflammatory Signaling:
Quan Zhou1, Qi Ouyang2, Hongli Wang1,3
1The State Key Laboratory for Artificial Microstructures and Mesoscopic Physics, School of Physics, Peking University, Beijing 100871, China.
Biomedicines
|July 28, 2026
Summary
Circadian disruption amplifies inflammation by altering immune system dynamics. This mathematical model explains how disrupted circadian rhythms prolong hyperinflammatory states, increasing disease risk.
Area of Science:
- Immunology
- Chronobiology
- Mathematical Biology
Background:
- Circadian disruption from jet lag, shift work, or aging increases inflammation and disease susceptibility.
- The precise mechanisms linking circadian disruption to exacerbated innate immune responses are not fully understood.
Purpose of the Study:
- To develop an integrated mathematical model of the circadian clock and innate immune responses.
- To elucidate the dynamical mechanisms by which circadian disruption impacts immune function.
Main Methods:
- Coupling of the mammalian circadian clock model with antigen-induced innate immune responses.
- Incorporation of key regulatory interactions like glucocorticoid modulation and pro-inflammatory feedback loops.
- Simulation of circadian disruption scenarios (jet lag, reduced clock gene amplitude).
Main Results:
- The model accurately reproduces experimental data on immune circadian oscillations and inflammatory response gating.
- Circadian gating functions by modulating bistability in pro-inflammatory feedback loops.
- Circadian disruption alters this bistable landscape, prolonging hyperinflammatory states.
Conclusions:
- Disrupted circadian rhythms amplify acute inflammatory responses and sustain chronic inflammation (inflammaging).
- This provides a mechanistic explanation for tissue injury and age-related inflammation linked to circadian disruption.
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