DetoxFungiV1, Main, Exploration, bibRecord, 000424

Ontogeny of alkaline phosphatase activity in infant intestines and breast milk.

Identifieur interne : 000424 ( Main/Exploration ); précédent : 000423; suivant : 000425

Ontogeny of alkaline phosphatase activity in infant intestines and breast milk.

Auteurs : Ye Yang [États-Unis] ; Emilee Rader [États-Unis] ; Michele Peters-Carr [États-Unis] ; Rebecca C. Bent [États-Unis] ; Jennifer T. Smilowitz [États-Unis] ; Karen Guillemin [États-Unis] ; Bethany Rader [États-Unis]

Source :

BMC pediatrics [ 1471-2431 ] ; 2019.

RBID : pubmed:30606146

Descripteurs français

KwdFr :
- Entérocolite nécrosante (étiologie), Humains (MeSH), Intestins (enzymologie), Lait humain (composition chimique), Lait humain (enzymologie), Nourrisson (MeSH), Nouveau-né (MeSH), Phosphatase alcaline (analyse), Phosphatase alcaline (métabolisme), Âge gestationnel (MeSH).
MESH :
- analyse : Phosphatase alcaline.
- composition chimique : Lait humain.
- enzymologie : Intestins, Lait humain.
- métabolisme : Phosphatase alcaline.
- étiologie : Entérocolite nécrosante.
- Humains, Nourrisson, Nouveau-né, Âge gestationnel.

English descriptors

KwdEn :
- Alkaline Phosphatase (analysis), Alkaline Phosphatase (metabolism), Enterocolitis, Necrotizing (etiology), Gestational Age (MeSH), Humans (MeSH), Infant (MeSH), Infant, Newborn (MeSH), Intestines (enzymology), Milk, Human (chemistry), Milk, Human (enzymology).
MESH :
- chemical , analysis : Alkaline Phosphatase.
- chemical , metabolism : Alkaline Phosphatase.
- chemistry : Milk, Human.
- enzymology : Intestines, Milk, Human.
- etiology : Enterocolitis, Necrotizing.
- Gestational Age, Humans, Infant, Infant, Newborn.

Abstract

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.

DOI: 10.1186/s12887-018-1379-1
PubMed: 30606146
PubMed Central: PMC6318838

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000609
to stream Main, to step Curation: 000609

Le document en format XML

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<series><title level="j">BMC pediatrics</title>
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<term>Alkaline Phosphatase (metabolism)</term>
<term>Enterocolitis, Necrotizing (etiology)</term>
<term>Gestational Age (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Infant (MeSH)</term>
<term>Infant, Newborn (MeSH)</term>
<term>Intestines (enzymology)</term>
<term>Milk, Human (chemistry)</term>
<term>Milk, Human (enzymology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Entérocolite nécrosante (étiologie)</term>
<term>Humains (MeSH)</term>
<term>Intestins (enzymologie)</term>
<term>Lait humain (composition chimique)</term>
<term>Lait humain (enzymologie)</term>
<term>Nourrisson (MeSH)</term>
<term>Nouveau-né (MeSH)</term>
<term>Phosphatase alcaline (analyse)</term>
<term>Phosphatase alcaline (métabolisme)</term>
<term>Âge gestationnel (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Alkaline Phosphatase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Alkaline Phosphatase</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Phosphatase alcaline</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Milk, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Lait humain</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Intestins</term>
<term>Lait humain</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Intestines</term>
<term>Milk, Human</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Enterocolitis, Necrotizing</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phosphatase alcaline</term>
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<term>Infant</term>
<term>Infant, Newborn</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>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.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>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.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>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.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>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.</p>
</div>
</front>
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<Abstract><AbstractText Label="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.</AbstractText>
<AbstractText Label="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.</AbstractText>
<AbstractText Label="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.</AbstractText>
<AbstractText Label="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.</AbstractText>
</Abstract>
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<AffiliationInfo><Affiliation>Institute of Molecular Biology, University of Oregon, Eugene, OR, USA.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Medicine, University of Florida, Gainesville, FL, USA.</Affiliation>
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</AffiliationInfo>
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	Serveur d'exploration sur la détoxication des champignons
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Ontogeny of alkaline phosphatase activity in infant intestines and breast milk.

Ontogeny of alkaline phosphatase activity in infant intestines and breast milk.

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