Immune system protein may defend against deadly intestinal disease in babies, study finds

A study led by researchers at Washington University School of Medicine in St. Louis has identified, in mice, a protein in the immune system that may protect babies from necrotizing enterocolitis (NEC) and lead to the development of new treatments.
The findings are published in the journal Cell Reports Medicine.
The intestinal disease necrotizing enterocolitis is a leading cause of death among premature infants born in the US and across the globe. Characterized by excessive inflammation that can cause tissue decay in the bowels, the disease provides a pathway for infectious and deadly bacteria to enter the bloodstream.
Despite four decades of research, effective treatments remain elusive, and mortality rates in babies who develop the disease have remained essentially unchanged, hovering at about 30%.
“Necrotizing enterocolitis is a serious, fast-acting condition that can lead to death within hours,” said the study’s senior author, Misty Good, MD, an assistant professor of paediatrics in the Division of Newborn Medicine.
“We don’t know why NEC happens, and we can try to treat it with antibiotics and surgical removal of the dead tissue; however, in severe cases, many babies will still die. No treatments stop the disease from progressing, but our hope is that the protein we’ve identified will change that.”
The scientists focused on Interleukin-22 (IL-22), a protein that regulates immune responses and helps maintain a healthy gut microbiome in adults.
Over the years, research has suggested that IL-22 has a critical role in adult gastrointestinal diseases. Consequently, potential treatments involving IL-22 are being studied in COVID-19 illness, alcohol-induced liver disease, and graft-versus-host disease that develops after organ or bone marrow transplants.
However, IL-22’s role in newborns’ intestines has been unclear. To better understand the protein’s role, the researchers created a mouse model to examine IL-22 signalling and production in healthy intestines and in intestines damaged by NEC. They analyzed IL-22 levels before and after birth and into adulthood, which for mice begins when they are weaned, at about 28 days old.
In both the healthy and diseased intestines, the researchers documented low postnatal IL-22 production up until day 21, when production skyrocketed for the mice and continued into adulthood.
The researchers also studied tissue samples from preemies who did and did not develop NEC. The scientists found low levels of IL-22 in all of the intestinal samples.
And in the babies who had developed NEC, an appropriate immune response had not been mounted in the intestines.
“Immune cells in the neonatal intestine have shown an inability to produce adequate amounts of IL-22 to control the progression of NEC,” said Good, who treats patients at St. Louis Children’s Hospital and is also co-program director of the university’s Neonatal-Perinatal Medicine Fellowship. (ANI)