Friday, 15 February 2013 19:20

Species Differences: Immune System Featured

A team of researchers led by Shaw Warren at Massachusetts General Hospital in Boston has investigated differences between the immune systems of humans and mice. The researchers discovered that the gene expression of white blood cells (leukocytes) in humans after various induced inflammatory diseases differs greatly to that of various strains of mice.

The scientists analysed blood samples from over 400 people who had suffered the inflammatory conditions of blunt force trauma, burns or bacterial toxins, as well as from healthy people. They analysed the gene transcript of leukocytes, which acts as a template for the expression of certain proteins for the body's reaction to the factor causing the disease, and then compared the transcripts with the blood cell reactions of three mouse models of a specific breed to comparable injuries.

The strain of mice used for these animal tests was C57 black 6, a temperamental strain that has a strong immune system, is easy to breed and is also well researched. The strain is commonly used for genetic manipulation. The scientists created so-called inflammation models by exposing the animals to the different inflammatory factors and then investigating the gene expression of their white blood cells, comparing them with the human results and conducting mathematical correlation analyses.

The researchers found out that there are only slight correlations in all three disease processes - trauma, burns and bacterial poisoning (inflammation caused by endotoxins). The signal pathways used by the body as a process for coping with the disease also differed considerably between humans and mice.

This casts new light on the results of animal models in research into inflammation and atherosclerosis, and their transferability to human conditions. The researchers advocate new approaches to research into human diseases, favouring the pathway approach. According to the researchers, the quality of animal models should be gauged by how well they can reflect the human disease on a molecular level, and not on a phenotype basis. With the aid of artificial in vitro human models, current disease models could be improved by reconstruction of the disease-relevant cell types or tissues.

http://www.spiegel.de/

Original publication:
Junhee Seok, et al. (2013): Genomic responses in mouse models poorly mimic human inflammatory diseases. PNAS early edition (http://www.pnas.org/cgi/doi/10.1073/pnas.1222878110)