Researchers from The University of Queensland’s Institute for Molecular Bioscience have uncovered a secret of an immune cell on the frontline that could assist with developing new treatments for inflammatory diseases.
“We have found that a type of immune cell doesn’t self-destruct like other cell types in our immunological army, and for this reason, it may be a key driver of inflammatory disease,” lead researcher Dr Kate Schroder said.
When bacteria enter our body, white blood cells—including neutrophils, macrophages and dendritic cells—are the first to scope out whether these bacteria pose a threat to our immune system.
If these white blood cells detect danger, clusters of molecules called inflammasomes are activated inside the cell.
Activating inflammasomes is like sounding the alarm for our immune system to begin a coordinated attack on the bacteria.
Dr Schroder said this attack is good thing in the case of infections, but inflammasomes are also activated by non-infectious signals, and having an inflammasome that remains activated for a prolonged period of time can result in excessive, unwanted inflammation.
“The inflammasome was only discovered about 10 years ago, and since then, a number of mutations in inflammasome molecules have been linked with genetic inflammatory diseases,” Dr Schroder said.
“Until now, most research on inflammasomes has been performed using macrophages and dendritic cells, which eventually self-destruct as a result of the activated inflammasomes.
“We found that in neutrophils, the activation of the inflammasome does not cause cell death, which means this type of white blood cell can hang around longer to fight off infectious agents.”
While this unique ability of neutrophils helps the body fight infections, because they don’t self-destruct like other cell types they continue to release inflammatory signals, which may lead to inflammatory disease in some settings.
Dr Schroder’s ongoing research into the inflammasome pathways and our immunological army has potential to help develop treatments for genetic and acquired inflammatory disease.
This research was published in Cell Reports and was supported by the National Health and Medical Research Council, the Australian Research Council and the Queensland Government.
Read more about Dr Schroder’s research here.
Media contact: IMB Communications on (07) 3346 2134 or communications@imb.uq.edu.au
