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Mouse models fail to mimic inflammatory genomic responses in Humans

Mouse models fail to mimic inflammatory genomic responses in Humans

In an article entitled, “Genomic responses in mouse models poorly mimic human inflammatory diseases,” published on February 26, 2013, issue of PNAS (110: 3507–3512), the lead author Junhee Seok with thirty eight other associates affiliated to eighteen research groups have reported on a systematic comparison of the genomic response between human inflammatory diseases and murine models. They confirmed that mouse models do not accurately reflect the genetic and proteomic responses to acute inflammatory stress in humans. They looked at burns, trauma and sepsis (infection in the blood). The researchers compared how human and mouse genes respond to certain types of trauma. They looked at gene activity in the blood of 167 people severely injured either by burns or by blunt trauma, such as in a car accident. They compared those results with gene activity in the blood of mice with similar injuries. The team also examined the reactions to an injection of endotoxin of four healthy men and 16 mice. When the researchers compared the gene activity changes in people with burns versus people with trauma, they found 97 percent similarity. For injuries and endotoxin exposure, 88 percent of gene responses were similar. But mouse responses were more varied. Compared with what goes on in humans, 47 to 63 percent of mouse genes changed activity in the same way. The result was not far from what researchers would expect from random chance. The results indicate that humans and mice react differently to traumas that often land people in intensive care units. The mouse immune system and the human immune system do not respond in the same way to stress. It helps to explain why every one of nearly 150 drugs tested at a huge expense in patients with sepsis has failed. The drug tests all were based on studies in mice. And mice, it turns out, can have something that looks like sepsis in humans, but is very different from the condition in humans. Consequently, drugs that are beneficial to mice and rats may or may not work in the same conditions in humans. The study shows that  the results from current models should be critically evaluated before being accepted as findings relevant to the human diseases may require new approaches  for the study of human diseases. [Summarized by Samsad Razzaque at the plant biotech lab., DU]

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