Helping Preterm Infants Fight Lung Infections May Start by Reinforcing Gut Microbiota
Published February 2020 | Immunity
Clinicians have worked for years to protect the under-developed lungs of preterm infants from devastating infections. Now, experts at Cincinnati Children’s report early signs of progress, in mice, at adjusting the gut-lung development axis to help preterm infants build healthier immune systems.
A team led by first author Katherine Oherle and senior author Hitesh Deshmukh, MD, PhD, has shed new light on the mechanisms at work as the lung’s alveoli begin to build their immune defenses. They found that the lung air sacs of preterm infants lack type 3 innate lymphoid cells crucial to responding to infection. They also found that production of these lymphoid cells depends on biological cues from commensal bacteria from the gut, specifically via production of the growth hormone IGF1.
Deleting pulmonary IGF1 in the lungs of newborn mice interrupted the development of type 3 innate lymphoid cells and made the mice susceptible to lung infections and pneumonia. The team also confirmed that a similar process occurs in humans.
The findings suggest that treating lungs directly with IGF1, or by stimulating healthy gut microbiota to generate IGF1, could help preterm infants develop stronger lungs. Both concepts will be evaluated in further studies.
“This study gives us important new information that helps us develop new and cost-effective methods to boost innate lung immunity in preterm babies. This could help them develop lifelong pulmonary resistance to respiratory infections,” Deshmukh says.
This discovery builds upon previous findings from Deshmukh and colleagues published in Nature Medicine (2014) and Science Translational Medicine (2017) that established the connection between commensal bacteria and lung immunity and warned of the long-term harm that can follow aggressive antibiotic regimens for premature infants.
