Despite advances in neonatal care, necrotizing enterocolitis (NEC) the most common gastrointestinal emergency in premature infants continues to be a deadly disease.
"We haven't made a lot of progress in identifying babies early who may be at risk for NEC, preventing it or treating it," said Jrn-Hendrik Weitkamp, M.D., a neonatologist and assistant professor of Pediatrics at Monroe Carell Jr. Children's Hospital at Vanderbilt.
Now, Weitkamp and his colleagues have discovered that disruptions in immune system regulation not previously considered to be important in NEC pathophysiology may play a role in the disease. The findings, reported in the journal Gut, suggest a new target for therapeutic interventions for NEC.
NEC is an inflammatory disease that kills intestinal tissue. Premature babies, and particularly those who have early formula feedings (breast milk has protective properties), are at increased risk for developing NEC.
About 40 percent of babies with NEC require surgery to remove dead bowel tissue and half of these babies do not survive. NEC survivors suffer long-term complications including bowel-related problems and impairments in motor and cognitive function.
Weitkamp wanted to explore whether differences in immune system regulation particularly in the "adaptive" immune response mediated by B cells and T cells might play a role in NEC. This type of cellular immunity was not considered important in the early neonatal period because it takes time to develop, and because it was not found in mouse models, Weitkamp said. But he knew from other studies that immune responses in newborn mice are not identical to immune responses in newborn humans.
Weitkamp and his colleagues turned to stored human intestinal tissue samples that had been surgically removed from preterm babies diagnosed with NEC or other intestinal diseases. They found high levels of T cells called T regulatory (Treg) cells in the i
|Contact: Leigh MacMillan|
Vanderbilt University Medical Center