Colostrum and Digestive Defense
Objective: We examined if human colostrum and milk contained pancreatic secretory trypsin inhibitor, a peptide of potential relevance for mucosal defence and using in vitro and in vivo models, determined if its presence influenced gut integrity and repair.
Designs: Human milk was collected from individuals over various times from parturition and PSTI concentrations determined using immunoassay. Human milk samples were analysed for proliferation & pro-migratory activity (wounded monolayers) and anti-apoptotic activity (caspase-3 activity) using intestinal HT29 cells +/- neutralizing antibodies to PSTI and EGF. Rats were restrained and given indomethacin to induce gastric injury. Effect of gavage with human breast milk +/- neutralizing antibodies on amount of injury were compared with animals receiving a commercial formula feed.
Results. PSTI is secreted into human milk with colostrum containing a much higher concentration of PSTI than human milk obtained later. Human milk stimulated migration and proliferation about three-fold and reduced indomethacin-induced apoptosis by about 70-80%. Sixty-five percent of the migratory effect of human milk could be removed by immunoneutralisation of PSTI. PSTI worked synergistically with EGF in mediating these effects. Gastric damage in rats was reduced by about 75% in the presence of human milk and was more efficacious than the formula feed (p<0·001). Protective effects of the milk were reduced by about 60% by PSTI immunoneutralisation.
Conclusions: PSTI is secreted into human milk at concentrations which have probable pathophysiological relevance.
From press release (June 30, 2009):
Magic Ingredient In Breast Milk Protects Babies' Intestines
Scientists at Queen Mary, University of London have discovered that an ingredient in human breast milk protects and repairs the delicate intestines of newborn babies.
The ingredient called pancreatic secretory trypsin inhibitor, or PSTI, is found at its highest levels in colostrum - the milk produced in the first few days after birth.
The lining of a newborn's gut is particularly vulnerable to damage as it has never been exposed to food or drink. The new study highlights the importance of breastfeeding in the first few days after the birth.
The researchers found small amounts of PSTI in all the samples of breast milk they tested but it was seven times more concentrated in colostrum samples. The ingredient was not found in formula milk.
The researchers examined the effects of PSTI on human intestinal cells in the lab. When they inflicted damage to the cells they found that PSTI stimulated the cells to move across the damaged area forming a natural protective 'plaster'. They also found that PSTI could prevent further damage by stopping the cells of the intestine from self-destructing. Additional research suggests that PSTI could reduce damage by 75 per cent.
PSTI is a molecule which is normally found in the pancreas where it protects the organ from being damaged by the digestive enzymes it produces. Research suggests that it plays a similar protective role in the gut.
The team at Queen Mary have also found that PSTI is produced in the breast but until now they did not know exactly why.
Professor Ray Playford of Barts and the London School of Medicine and Dentistry, part of Queen Mary, University of London led the study.
He said: "We know that breast milk is made up of a host of different ingredients and we also know that there are a number of health benefits for babies who are breast-fed.
"This study is important because it shows that a component of breast milk protects and repairs the babies delicate intestines in readiness for the onslaught of all the food and drink that are to come.
"It reinforces the benefits of breast feeding, especially in the first few days after birth."
Tania Marchbank, Gillian Weaver, Marit Nilsen-Hamilton, and Raymond J Playford.
Pancreatic secretory trypsin inhibitor is a major motogenic and protective factor in human breast milk.
Am J Physiol Gastrointest Liver Physiol
Institute of Cell and Molecular Science, Barts & The London School of Medicine, Queen Mary, University of London.