Inflammatory signals activate Nuclear Factor kappa B proteins to start a clock ticking where Nuclear Factor kappa B proteins move forwards and backwards in and out of the cell nucleus switching genes on and off. This process gives the cell ability to respond to wound, infection, and tumors. When Nuclear Factor kappa B proteins go uncontrolled it is associated with inflammatory diseases.
At 34 degrees body temperature Nuclear Factor kappa B protein clock slows down. Temperatures higher than normal 37 degree body temperatures triggers the Nuclear Factor kappa B protein clock to speed up, as in with fever. Mathematicians calculated how temperature increases speed the cycle up, and predicted that A20 protein which is critical to avoid inflammatory disease is essential to this process; when A20 was removed from cells it was found that NF-kB clock lost sensitivity to temperature increases.
Many activities of many Nuclear Factor kappa B proteins controlled genes are not affected by temperature, key groups of genes showed altered profiles at different temperatures. Temperature sensitivity genes included important inflammatory controllers and regulators of cell communication that alter cell responses.
Influenza and cold epidemics tend to do better and become worse in winter when temperatures are cooler, model mice living in higher temperatures suffer less from inflammation and cancer, these changes can now be explained by altered immune responses at different temperatures, according to the researchers.
Temperature changes within the body have been shown by this study to change inflammation cells and tissues in a biologically organised manner, and suggests that new drug may precisely change inflammatory responses by targeting A20 proteins.
