An act of handbrake on the immune system's runaway reaction to flu infection can be acted by a protein called SOCS4 by providing a possible means of minimising the impact of flu pandemics.
Scientists from Melbourne's Walter and Eliza Hall Institute have found that without SOCS4 the immune response to influenza infection is slowed and there is a vast increase in the number of damaging inflammatory molecules in the lungs.
AdvertisementThis flood of inflammatory molecules, known as a 'cytokine storm', is thought to contribute to flu-related deaths in humans.
Dr Lukasz Kedzierski, Dr Sandra Nicholson and colleagues from the institute, in collaboration with Associate Professor Katherine Kedzierska and colleagues from The University of Melbourne, made the discovery.
Suppressors of cytokine signalling (SOCS) molecules control the flow of chemical messages inside cells and were discovered by institute researchers in the 1990s. Immune cells release signalling molecules called cytokines to trigger an immune response that protects the body from infection.
If too many cytokines are released, SOCS proteins suppress the activity of the cytokines to prevent unwanted inflammation and tissue damage.
Dr Kedzierski said removing SOCS4 upset the normal immune response to influenza infection.
A cytokine storm could result in increased severity of symptoms and, in many instances, to multiple organ failure and death, Dr Kedzierski said. "A cytokine storm is like an uncontrolled chain reaction, and the cytokines that normally stimulate the immune response continue to trigger other immune cells to produce more cytokines. Our research suggests that SOCS4 keeps this response under control, preventing a cytokine storm in the lungs that can lead to a build up of fluid that restricts breathing and can ultimately result in death."
Dr Nicholson said drugs that enhanced or mimicked SOCS4 action could be a useful way of treating pandemic or more aggressive flu strains, as well as other infections.
The study has been published in the journal PLOS Pathogens.