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NIH investigators find link between DNA damage and immune response
Date:3/31/2011

Researchers offer the first evidence that DNA damage can lead to the regulation of inflammatory responses, the body's reaction to injury. The proteins involved in the regulation help protect the body from infection.

The study, performed by scientists at the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health, is one of the first studies to come out of the recently established NIEHS Clinical Research Unit (CRU) (http://www.niehs.nih.gov/research/clinical/join/durham/index.cfm).

Appearing in the March 31 issue of PLoS Genetics, the research suggests that an injury to chromosomes alters the expression of a family of genes known as Toll-like receptors (TLRs). TLRs are proteins that play a role in the immune system by defending the body from infection. Following damage, the TLRs interact with the tumor suppressor gene p53 to regulate the amount of inflammation. The NIEHS investigators also establish that the integration of p53 and inflammation only occurs in primates.

Healthy volunteers with informed consent donated their blood cells for the study. The scientists separated white blood cells from the samples and exposed the cells to anti-cancer agents to activate p53. They then examined the expression of TLR genes. The team detected large variations among individuals, but found that p53 generally led to the activation of several TLR genes in patients' cells. They also found that TLR activation could be prevented by adding the p53 inhibitor pifithrin.

"We would not have found this connection if we only worked with rat or mice cells," said Michael Resnick, Ph.D., principal investigator in the Laboratory of Molecular Genetics (LMG) and corresponding author on the paper. "We needed to have human samples, so our collaboration with the CRU was crucial for these experiments."

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Contact: Robin Arnette
arnetter@niehs.nih.gov
919-541-5143
NIH/National Institute of Environmental Health Sciences
Source:Eurekalert

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