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Ontogeny of alkaline phosphatase activity in infant intestines and breast milk
Ye Yang1,2, Emilee Rader3, Michele Peters-Carr4
1Institute of Molecular Biology, University of Oregon, Eugene, OR, USA.
Insights
Necrotizing enterocolitis (NEC) is linked to low alkaline phosphatase (ALP) activity in premature infants. Both preterm birth and limited breast milk feeding reduce ALP levels, impairing the infant
Area of Science:
- Neonatal Medicine
- Gastroenterology
- Biochemistry
Background:
- Necrotizing enterocolitis (NEC) is a severe intestinal inflammatory condition affecting premature infants.
- Exposure to bacterial products like lipopolysaccharide is a risk factor for NEC.
- Alkaline phosphatase (ALP) can mitigate lipopolysaccharide-induced inflammation, and premature infants show reduced ALP activity.
Purpose of the Study:
- To investigate the alkaline phosphatase (ALP) activity in the premature neonatal intestine.
- To determine if meconium ALP activity correlates with gestational age.
- To assess breast milk as a source of exogenous ALP for neonates.
Main Methods:
- Quantified ALP activity in 122 meconium samples (24-40 weeks gestational age).
- Measured ALP activity in 289 breast milk samples from 78 mothers (days 2-49 post-birth).
Main Results:
- Meconium ALP activity showed a positive correlation with gestational age; preterm infants had lower activity.
- Breast milk ALP activity peaked at day 2 post-birth, declining over the subsequent weeks.
Conclusions:
- Preterm birth is associated with lower endogenous intestinal ALP activity.
- Reduced breast milk ALP levels in early infancy may also contribute to NEC risk.
- Paucity of ALP activity impairs the infant's ability to detoxify harmful bacterial products, increasing NEC susceptibility.
Background:
Necrotizing enterocolitis (NEC) is a devastating disease of intestinal inflammation that primarily affects premature infants. A potential risk factor for necrotizing enterocolitis is exposure of the premature neonatal intestine to environmental bacteria and their proinflammatory products such as lipopolysaccharide. The metalloenzyme alkaline phosphatase (ALP) has been shown to reduce lipopolysaccharide-mediated inflammation. Additionally, premature rat pups have reduced alkaline phosphatase activity and expression as compared to full term pups. To explore the possibility that the human premature neonatal intestine has a paucity of alkaline phosphatase activity, we measured endogenously produced intestinal alkaline phosphatase activity in meconium as a function of gestational age. To test whether breast milk could serve as a source of exogenous alkaline phosphatase to the neonatal intestine through ingestion, we measured alkaline phosphatase activity in breast milk across a range of time points post-birth.
Methods:
Alkaline phosphatase activity was quantified in 122 meconium samples from infants of gestational ages ranging from 24 to 40 weeks and in 289 breast milk samples collected from 78 individual mothers between days 2-49 post-birth.
Results:
We observed a strong positive correlation between the meconium alkaline phosphatase activity and gestational age, with preterm infants having lower meconium alkaline phosphatase activities than early term or term infants. Breast milk alkaline phosphatase activity was highest in the first week post-birth, with peak alkaline phosphatase activity at day 2 post-birth, followed by relatively low alkaline phosphatase activity in weeks 2-7.
Conclusions:
Our results are consistent with the two major risk factors for necrotizing enterocolitis development, preterm birth and lack of breast milk feeding, both contributing to a paucity of alkaline phosphatase activity and impaired capacity to detoxify proinflammatory bacterial products such as lipopolysaccharide.
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