Brisbane scientists have discovered why children who were hospitalised with a severe viral respiratory infections as babies are more likely to develop asthma.
The head of QIMR Berghofer Medical Research Institute’s Respiratory Immunology laboratory, Associate Professor Simon Phipps, said the research could pave the way for the development of an early preventative treatment to stop the onset of asthma in children.
The findings have been published today in the journal Science Translational Medicine.
Associate Professor Phipps said severe viral respiratory infections in infants were associated with a higher risk of developing asthma by the age of five.
He said for the first time scientists were able to identify why that was.
“We have been able to show that young mice with a respiratory virus produce a cell messenger called prostaglandin 2 that actually makes it harder for their immune system to clear the viral infection,” he said.
“In our studies, the prostaglandin 2 messenger played a role in turning down the production of anti-viral proteins.
“We found that if we blocked the cell messenger prostaglandin 2 from reaching its target, the mice were able to clear the virus more quickly.”
Associate Professor Phipps said his group validated the findings by demonstrating that the levels of prostaglandin 2 were higher in the upper airways of babies hospitalised with the respiratory virus.
He said researchers then tested the cell messenger in the laboratory using human epithelial cells, which line the airways.
“When we infected the cells with the virus in the laboratory, it increased the enzyme that produces the cell messenger prostaglandin 2 and therefore increased the amount of prostaglandin 2 overall,” he said.
“When we blocked the ability of the cell messenger to reach its target, the virus was again able to be cleared more quickly.
“This particular type of cell messenger has been linked to driving allergic inflammation in asthma.
“Our research suggests that in addition to stopping the bad inflammation caused by the prostaglandin 2, blocking it also restores the immune system’s ability to fight a viral infection and reduces the risk of an asthma attack, which is often triggered by viral infection.”
Associate Professor Phipps said respiratory syncytial virus infections caused 200,000 deaths worldwide each year, mainly in children under five.
He said the identification of the cell messenger prostaglandin 2 as playing a key role in the development of bronchiolitis and asthma could lead to the development of new drug targets.
“We didn’t know previously that this particular cell messenger was involved in suppressing the immune system of infants with respiratory viruses,” he said.
“If we block this cell messenger from reaching its target, we now believe that infants will have a better chance of clearing the virus and rates of illness should reduce.
“We also believe that blocking it could help to reduce the risk of a child developing asthma later in life.”
Associate Professor Phipps said there was even potential to investigate early preventative treatments.
“Our understanding of why kids get asthma is becoming clearer. Asthma risk is much higher where a child had a severe viral infection as a baby,” he said.
“If we can identify those infants early and administer a treatment that blocks the production of the cell messenger prostaglandin 2, we can help them get better faster, and potentially avoid a future diagnosis of asthma.
“This is still a long way from being developed into a treatment for human infants, but it is a significant and exciting first step.”
The Brisbane-led research involved collaborators from across Australia and New Zealand.
Associate Professor Phipps’s research was supported by an Australian Infectious Disease Research Excellence award, an NHMRC grant, and an Australian Research Council Future Fellowship.