The hotter your body, lesser you are prone to infection, wound and tumors.
A new research led by the researchers at the Universities of Warwick and Manchester demonstrated that little rise in temperature of your body fastens the cellular clock whose function is to turn the gene on and off in response to infection.
This new finding can help researchers to produce a drug which is fast working as well as effective, and target the key inflammation protein which is important for temperature response
During their research, scientists found that inflammatory signals activate ‘Nuclear Factor kappa B’ (NF-κB) proteins which in turn starts a clock ticking in which NF-κB proteins move backward and forwards into and out of the cell nucleus, where they switch genes on and off.
This activation permits the cell to respond to a tumor, wound or infection. If NF-κB proteins are irregulated it leads to many inflammatory diseases like Crohn’s disease, psoriasis, and rheumatoid arthritis.
During their study researchers analyzed that At a body temperature of 34 degrees, the NF-κB clock slows down and on increasing the body temperatures than the normal 37-degree body temperature (such as in fever, 40 degrees), the NF-κB clock speeds up.
Mathematicians at the University of Warwick’s Systems Biology Centre calculated how temperature increases make the cycle speed up.
The researchers found that the protein which is necessary to avoid inflammation is involved in this process. This protein was called as A20. To confirm it, they removed the protein from the cell which leads to the finding that NF-kB clock lost its sensitivity increases in temperature.
He commented: “the lower body temperature during sleep might provide a fascinating explanation of how shift work, jet lag or sleep disorders cause increased inflammatory disease”
Mathematician Dan Woodcock from the University of Warwick said: “this is a good example of how mathematical modeling of cells can lead to useful new biological understanding.”
The effect of temperature was not noticed on the activities of many NF-kB controlled genes, but a key group of genes showed altered profiles at the different temperatures. These temperature sensitive genes included key inflammatory regulators and controllers of cell communication that can alter cell responses.
With this study in mind, researchers concluded that the temperature changes inflammation in cells and tissues in a biologically organized way and gives a hope that new drugs might more precisely change the inflammatory response by targeting the A20 protein.
Professor Mike White, the lead biologist from the University of Manchester, said the study provides a possible explanation of how both environmental and body temperature affects our health:
“We have known for some time that influenza and cold epidemics tend to be worse in the winter when temperatures are cooler. Also, mice living at higher temperatures suffer less from inflammation and cancer. These changes may now be explained by altered immune responses at different temperatures.”