SCIENCE CORNER

Are Mice Just Bad Models of Inflammation?  
Or do the results of a new study have broader implications?

February 22, 2013
Dr. Pam Osenkowski, NAVS Director of Science Programs


Game changer. These are the words that summarized the findings of a recent study on inflammation, the body’s response to injury. The results of the first systematic evaluation of how well mouse models mimic inflammatory diseases in human patients at the molecular level were published earlier this month. The study is receiving a lot of media attention because researchers are “blown away” by how poorly mice model these human conditions and are “stunned by just how bad the mouse data are.”  The study determined that there is very little overlap in the genes that humans and mice use to handle things like trauma, burns, and bacterial toxins -- even though both species have equivalent versions of those genes.  This new study provides an explanation for why 150 drugs that could successfully treat a sepsis-like condition in mice failed in human patients, at the expense of years of time and billions of research dollars.

For decades, scientists have traditionally relied on animal models in their efforts to uncover the mysteries of health and disease.  While there have always been difficulties in extrapolating data from animals to people, researchers had convinced the public, and themselves, that they were on the right track, and that results from animal models could be translated directly to humans.  But if animals are great models for humans, why have drugs that have cured ailments in those animals failed in humans?  Researchers have too often focused on the similarities between animal models and people when they really should have spent more time on understanding the differences.  Advances in science and technology now allow researchers to appreciate the differences between species, especially those at the molecular level, and have painted a clearer picture of why animal models are poorly predictive of human conditions. Just because animal models may appear to mimic human conditions on the surface, the molecular behavior of the relevant genes and pathways critical for human disease is not the same.

This “game changing” study reinforces the message that NAVS has long voiced: scientific evidence shows that the use of animals in science can mislead researchers while it wastes valuable time and resources. The scientific community should move beyond the inherently problematic methodology of animal models. Researchers need to re-direct their efforts to explore more human-relevant ways to answer the scientific questions of today.  

As Kenny Rogers said, "You got to know when to hold 'em, know when to fold 'em, know when to walk away and when to run."  As a scientist I can say it's time to fold on animal models and run toward more human-relevant models if we truly want to answer the scientific questions of today.  And while Dr. Francis Collins, Director of the NIH, may not agree with my assessment to "fold" on animal models altogether, he definitely sees the value in running toward more human-relevant systems. As he stated, “The new study provides more reason to develop better and more sophisticated models of human disease.”  New and improved in vitro systems, like the organ-on-a-chip we've discussed in the Science portion of the NAVS website according to Dr. Collins “may ultimately provide better models of human disease and biology than the use of animals.”

Researchers in the field of inflammation have gotten the ball rolling and have identified the importance of understanding if animal models actually mimic human conditions at the molecular level.   I have no doubt that the implications of this study will become much more widespread, as researchers in other disease fields will also begin to question the adequacy of their own animal models, and upon examination, might very well find the same thing.  In any case, it is clear that future advances in the field of inflammatory disease will only come from the generation of human-relevant in vitro systems and information obtained from human patients.  It is time to shift gears and reset research priorities before we waste more time and research dollars on animal models that we know scientifically just don't work.

References:Genomic responses in mouse models poorly mimic human inflammatory diseases. Seok J, et al. Proc Natl Acad Sci U S A. 2013 Feb 11.
 
 
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53 West Jackson Blvd., Suite 1552
Chicago, IL 60604
(800) 888-NAVS or (312) 427-6065
Fax: (312) 427-6524
navs@navs.org
© 2013 National Anti-Vivisection Society is a
501(c)3 non-profit organization