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Updated: May 14, 2026
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Genomic responses in mouse models poorly mimic human inflammatory diseases
Junhee Seok1, H Shaw Warren, Alex G Cuenca
1Stanford Genome Technology Center, Stanford University, Palo Alto, CA 94305, USA.
Abstract:
A cornerstone of modern biomedical research is the use of mouse models to explore basic pathophysiological mechanisms, evaluate new therapeutic approaches, and make go or no-go decisions to carry new drug candidates forward into clinical trials. Systematic studies evaluating how well murine models mimic human inflammatory diseases are nonexistent. Here, we show that, although acute inflammatory stresses from different etiologies result in highly similar genomic responses in humans, the responses in corresponding mouse models correlate poorly with the human conditions and also, one another. Among genes changed significantly in humans, the murine orthologs are close to random in matching their human counterparts (e.g., R(2) between 0.0 and 0.1). In addition to improvements in the current animal model systems, our study supports higher priority for translational medical research to focus on the more complex human conditions rather than relying on mouse models to study human inflammatory diseases.
Insights
Mouse models poorly mimic human inflammatory diseases, showing random gene response correlation. Future research should prioritize complex human conditions over animal models for better translational medicine outcomes.
Area of Science:
- Biomedical Research
- Translational Medicine
- Genomics
Background:
- Mouse models are crucial for understanding disease and testing therapies.
- Current mouse models for inflammatory diseases lack systematic evaluation for human mimicry.
Purpose of the Study:
- To assess the correlation between genomic responses in mouse models and human inflammatory diseases.
- To evaluate the reliability of mouse models in preclinical research.
Main Methods:
- Comparative genomic analysis of human and mouse responses to acute inflammatory stress.
- Statistical assessment of gene ortholog expression correlation (R-squared values).
Main Results:
- Human inflammatory responses to diverse stresses show high genomic similarity.
- Mouse models exhibit poor correlation with human inflammatory disease genomic profiles (R-squared 0.0-0.1).
- Murine ortholog gene responses poorly matched human counterparts.
Conclusions:
- Current mouse models inadequately replicate human inflammatory disease genetics.
- Improvements in animal models are needed.
- Translational research should increase focus on human conditions rather than mouse models.
