Exploring the Immunomodulatory Potential of Human Milk: Aryl Hydrocarbon Receptor Activation and Its Impact on Neonatal Gut Health
Several metabolites of the essential amino acid tryptophan have emerged as key players in gut homeostasis through different cellular pathways, particularly through metabolites which can activate the aryl hydrocarbon receptor (AHR). This study aimed to map the metabolism of tryptophan in early life a...
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| Veröffentlicht in: | Nutrients 2024-05, Vol.16 (10), p.1531 |
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| creator | Wieser, Naomi V Ghiboub, Mohammed Verseijden, Caroline van Goudoever, Johannes B Schoonderwoerd, Anne de Meij, Tim G J Niemarkt, Hendrik J Davids, Mark Lefèvre, Antoine Emond, Patrick Derikx, Joep P M Jonge, Wouter J de Sovran, Bruno |
| description | Several metabolites of the essential amino acid tryptophan have emerged as key players in gut homeostasis through different cellular pathways, particularly through metabolites which can activate the aryl hydrocarbon receptor (AHR). This study aimed to map the metabolism of tryptophan in early life and investigate the effects of specific metabolites on epithelial cells and barrier integrity. Twenty-one tryptophan metabolites were measured in the feces of full-term and preterm neonates as well as in human milk and formula. The ability of specific AHR metabolites to regulate cytokine-induced IL8 expression and maintain barrier integrity was assessed in Caco2 cells and human fetal organoids (HFOs). Overall, higher concentrations of tryptophan metabolites were measured in the feces of full-term neonates compared to those of preterm ones. Within AHR metabolites, indole-3-lactic acid (ILA) was significantly higher in the feces of full-term neonates. Human milk contained different levels of several tryptophan metabolites compared to formula. Particularly, within the AHR metabolites, indole-3-sulfate (I3S) and indole-3-acetic acid (IAA) were significantly higher compared to formula. Fecal-derived ILA and milk-derived IAA were capable of reducing TNFα-induced IL8 expression in Caco2 cells and HFOs in an AHR-dependent manner. Furthermore, fecal-derived ILA and milk-derived IAA significantly reduced TNFα-induced barrier disruption in HFOs. |
| doi_str_mv | 10.3390/nu16101531 |
| format | Article |
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This study aimed to map the metabolism of tryptophan in early life and investigate the effects of specific metabolites on epithelial cells and barrier integrity. Twenty-one tryptophan metabolites were measured in the feces of full-term and preterm neonates as well as in human milk and formula. The ability of specific AHR metabolites to regulate cytokine-induced IL8 expression and maintain barrier integrity was assessed in Caco2 cells and human fetal organoids (HFOs). Overall, higher concentrations of tryptophan metabolites were measured in the feces of full-term neonates compared to those of preterm ones. Within AHR metabolites, indole-3-lactic acid (ILA) was significantly higher in the feces of full-term neonates. Human milk contained different levels of several tryptophan metabolites compared to formula. Particularly, within the AHR metabolites, indole-3-sulfate (I3S) and indole-3-acetic acid (IAA) were significantly higher compared to formula. Fecal-derived ILA and milk-derived IAA were capable of reducing TNFα-induced IL8 expression in Caco2 cells and HFOs in an AHR-dependent manner. Furthermore, fecal-derived ILA and milk-derived IAA significantly reduced TNFα-induced barrier disruption in HFOs.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu16101531</identifier><identifier>PMID: 38794769</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acetic acid ; aryl hydrocarbon receptors ; Basic Helix-Loop-Helix Transcription Factors ; breast milk ; Caco-2 Cells ; Calibration ; Cytokines ; digestive system ; epithelium ; essential amino acids ; Feces ; Feces - chemistry ; Female ; homeostasis ; Humans ; Hydrocarbons ; Immunomodulators ; indole acetic acid ; Indoleacetic Acids - analysis ; Indoleacetic Acids - metabolism ; Infant Formula - chemistry ; Infant, Newborn ; Infant, Premature ; Infants (Premature) ; Inflammation ; interleukin-8 ; Interleukin-8 - metabolism ; Ligands ; Metabolism ; Metabolites ; Microbiota ; Milk ; Milk, Human - chemistry ; Milk, Human - metabolism ; organoids ; Organoids - metabolism ; Premature birth ; Receptors, Aryl Hydrocarbon - metabolism ; Scientific equipment and supplies industry ; Sepsis ; Serotonin ; Sulfates ; Tryptophan ; Tryptophan - analysis ; Tryptophan - metabolism</subject><ispartof>Nutrients, 2024-05, Vol.16 (10), p.1531</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-3672f84a39db623924d9ca5019b87f834ba6576126bf77a03c492a86d23dade93</citedby><cites>FETCH-LOGICAL-c451t-3672f84a39db623924d9ca5019b87f834ba6576126bf77a03c492a86d23dade93</cites><orcidid>0000-0003-3081-9124 ; 0000-0003-3960-1703 ; 0000-0002-0844-7208 ; 0000-0002-2095-371X ; 0000-0002-5324-2164 ; 0000-0002-3241-1547</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38794769$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wieser, Naomi V</creatorcontrib><creatorcontrib>Ghiboub, Mohammed</creatorcontrib><creatorcontrib>Verseijden, Caroline</creatorcontrib><creatorcontrib>van Goudoever, Johannes B</creatorcontrib><creatorcontrib>Schoonderwoerd, Anne</creatorcontrib><creatorcontrib>de Meij, Tim G J</creatorcontrib><creatorcontrib>Niemarkt, Hendrik J</creatorcontrib><creatorcontrib>Davids, Mark</creatorcontrib><creatorcontrib>Lefèvre, Antoine</creatorcontrib><creatorcontrib>Emond, Patrick</creatorcontrib><creatorcontrib>Derikx, Joep P M</creatorcontrib><creatorcontrib>Jonge, Wouter J de</creatorcontrib><creatorcontrib>Sovran, Bruno</creatorcontrib><title>Exploring the Immunomodulatory Potential of Human Milk: Aryl Hydrocarbon Receptor Activation and Its Impact on Neonatal Gut Health</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Several metabolites of the essential amino acid tryptophan have emerged as key players in gut homeostasis through different cellular pathways, particularly through metabolites which can activate the aryl hydrocarbon receptor (AHR). This study aimed to map the metabolism of tryptophan in early life and investigate the effects of specific metabolites on epithelial cells and barrier integrity. Twenty-one tryptophan metabolites were measured in the feces of full-term and preterm neonates as well as in human milk and formula. The ability of specific AHR metabolites to regulate cytokine-induced IL8 expression and maintain barrier integrity was assessed in Caco2 cells and human fetal organoids (HFOs). Overall, higher concentrations of tryptophan metabolites were measured in the feces of full-term neonates compared to those of preterm ones. Within AHR metabolites, indole-3-lactic acid (ILA) was significantly higher in the feces of full-term neonates. Human milk contained different levels of several tryptophan metabolites compared to formula. Particularly, within the AHR metabolites, indole-3-sulfate (I3S) and indole-3-acetic acid (IAA) were significantly higher compared to formula. Fecal-derived ILA and milk-derived IAA were capable of reducing TNFα-induced IL8 expression in Caco2 cells and HFOs in an AHR-dependent manner. Furthermore, fecal-derived ILA and milk-derived IAA significantly reduced TNFα-induced barrier disruption in HFOs.</description><subject>Acetic acid</subject><subject>aryl hydrocarbon receptors</subject><subject>Basic Helix-Loop-Helix Transcription Factors</subject><subject>breast milk</subject><subject>Caco-2 Cells</subject><subject>Calibration</subject><subject>Cytokines</subject><subject>digestive system</subject><subject>epithelium</subject><subject>essential amino acids</subject><subject>Feces</subject><subject>Feces - chemistry</subject><subject>Female</subject><subject>homeostasis</subject><subject>Humans</subject><subject>Hydrocarbons</subject><subject>Immunomodulators</subject><subject>indole acetic acid</subject><subject>Indoleacetic Acids - analysis</subject><subject>Indoleacetic Acids - metabolism</subject><subject>Infant Formula - chemistry</subject><subject>Infant, Newborn</subject><subject>Infant, Premature</subject><subject>Infants (Premature)</subject><subject>Inflammation</subject><subject>interleukin-8</subject><subject>Interleukin-8 - 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| ispartof | Nutrients, 2024-05, Vol.16 (10), p.1531 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Acetic acid aryl hydrocarbon receptors Basic Helix-Loop-Helix Transcription Factors breast milk Caco-2 Cells Calibration Cytokines digestive system epithelium essential amino acids Feces Feces - chemistry Female homeostasis Humans Hydrocarbons Immunomodulators indole acetic acid Indoleacetic Acids - analysis Indoleacetic Acids - metabolism Infant Formula - chemistry Infant, Newborn Infant, Premature Infants (Premature) Inflammation interleukin-8 Interleukin-8 - metabolism Ligands Metabolism Metabolites Microbiota Milk Milk, Human - chemistry Milk, Human - metabolism organoids Organoids - metabolism Premature birth Receptors, Aryl Hydrocarbon - metabolism Scientific equipment and supplies industry Sepsis Serotonin Sulfates Tryptophan Tryptophan - analysis Tryptophan - metabolism |
| title | Exploring the Immunomodulatory Potential of Human Milk: Aryl Hydrocarbon Receptor Activation and Its Impact on Neonatal Gut Health |
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