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Modulation of DNA methylation states and infant immune system by dietary supplementation with ω-3 PUFA during pregnancy in an intervention study12345

Identifieur interne : 001305 ( Ncbi/Merge ); précédent : 001304; suivant : 001306

Modulation of DNA methylation states and infant immune system by dietary supplementation with ω-3 PUFA during pregnancy in an intervention study12345

Auteurs : Ho-Sun Lee ; Albino Barraza-Villarreal ; Hector Hernandez-Vargas ; Peter D. Sly ; Carine Biessy ; Usha Ramakrishnan ; Isabelle Romieu ; Zdenko Herceg

Source :

The American Journal of Clinical Nutrition [ 0002-9165 ] ; 2013.

RBID : PMC:3712555

Abstract

Background: Early-life exposures to tobacco smoke and some dietary factors have been identified to induce epigenetic changes in genes involved in allergy and asthma development. Omega-3 (n−3) polyunsaturated fatty acid (PUFA) intake during pregnancy could modulate key cytokines and T helper (Th) cell maturation; however, little is known about the mechanism by which ω-3 PUFA could have a beneficial effect in preventing inflammatory disorders.

Objective: We sought to test whether prenatal dietary supplementation with ω-3 PUFA during pregnancy may modulate epigenetic states in the infant immune system.

Design: This study was based on a randomized intervention trial conducted in Mexican pregnant women supplemented daily with 400 mg docosahexaenoic acid (DHA) or a placebo from 18 to 22 wk of gestation to parturition. We applied quantitative profiling of DNA methylation states in Th1, Th2, Th17, and regulatory T–relevant genes as well as LINE1 repetitive elements of cord blood mononuclear cells (n = 261).

Results: No significant difference in promoter methylation levels was shown between ω-3 PUFA–supplemented and control groups for the genes analyzed; however, ω-3 PUFA supplementation was associated with changes in methylation levels in LINE1 repetitive elements (P = 0.03) in infants of mothers who smoked during pregnancy. Furthermore, an association between the promoter methylation levels of IFNγ and IL13 was modulated by ω-3 PUFA supplementation (P = 0.06).

Conclusions: Our results indicate that maternal supplementation with ω-3 PUFA during pregnancy may modulate global methylation levels and the Th1/Th2 balance in infants. Therefore, the epigenetic mechanisms could provide attractive targets for prenatal modulation and prevention of inflammatory disorders and potentially other related diseases in childhood and adulthood.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712555

DOI: 10.3945/ajcn.112.052241
PubMed: 23761484
PubMed Central: 3712555

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PMC:3712555

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<author><name sortKey="Barraza Villarreal, Albino" sort="Barraza Villarreal, Albino" uniqKey="Barraza Villarreal A" first="Albino" last="Barraza-Villarreal">Albino Barraza-Villarreal</name>
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<author><name sortKey="Hernandez Vargas, Hector" sort="Hernandez Vargas, Hector" uniqKey="Hernandez Vargas H" first="Hector" last="Hernandez-Vargas">Hector Hernandez-Vargas</name>
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<author><name sortKey="Ramakrishnan, Usha" sort="Ramakrishnan, Usha" uniqKey="Ramakrishnan U" first="Usha" last="Ramakrishnan">Usha Ramakrishnan</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Modulation of DNA methylation states and infant immune system by dietary supplementation with ω-3 PUFA during pregnancy in an intervention study<xref ref-type="aff" rid="aff1"><sup>1</sup>
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<author><name sortKey="Lee, Ho Sun" sort="Lee, Ho Sun" uniqKey="Lee H" first="Ho-Sun" last="Lee">Ho-Sun Lee</name>
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<author><name sortKey="Barraza Villarreal, Albino" sort="Barraza Villarreal, Albino" uniqKey="Barraza Villarreal A" first="Albino" last="Barraza-Villarreal">Albino Barraza-Villarreal</name>
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<author><name sortKey="Hernandez Vargas, Hector" sort="Hernandez Vargas, Hector" uniqKey="Hernandez Vargas H" first="Hector" last="Hernandez-Vargas">Hector Hernandez-Vargas</name>
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<author><name sortKey="Sly, Peter D" sort="Sly, Peter D" uniqKey="Sly P" first="Peter D" last="Sly">Peter D. Sly</name>
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<author><name sortKey="Biessy, Carine" sort="Biessy, Carine" uniqKey="Biessy C" first="Carine" last="Biessy">Carine Biessy</name>
</author>
<author><name sortKey="Ramakrishnan, Usha" sort="Ramakrishnan, Usha" uniqKey="Ramakrishnan U" first="Usha" last="Ramakrishnan">Usha Ramakrishnan</name>
</author>
<author><name sortKey="Romieu, Isabelle" sort="Romieu, Isabelle" uniqKey="Romieu I" first="Isabelle" last="Romieu">Isabelle Romieu</name>
</author>
<author><name sortKey="Herceg, Zdenko" sort="Herceg, Zdenko" uniqKey="Herceg Z" first="Zdenko" last="Herceg">Zdenko Herceg</name>
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<series><title level="j">The American Journal of Clinical Nutrition</title>
<idno type="ISSN">0002-9165</idno>
<idno type="eISSN">1938-3207</idno>
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<front><div type="abstract" xml:lang="en"><p><bold>Background:</bold>
 Early-life exposures to tobacco smoke and some dietary factors have been identified to induce epigenetic changes in genes involved in allergy and asthma development. Omega-3 (n−3) polyunsaturated fatty acid (PUFA) intake during pregnancy could modulate key cytokines and T helper (Th) cell maturation; however, little is known about the mechanism by which ω-3 PUFA could have a beneficial effect in preventing inflammatory disorders.</p>
<p><bold>Objective:</bold>
 We sought to test whether prenatal dietary supplementation with ω-3 PUFA during pregnancy may modulate epigenetic states in the infant immune system.</p>
<p><bold>Design:</bold>
 This study was based on a randomized intervention trial conducted in Mexican pregnant women supplemented daily with 400 mg docosahexaenoic acid (DHA) or a placebo from 18 to 22 wk of gestation to parturition. We applied quantitative profiling of DNA methylation states in Th1, Th2, Th17, and regulatory T–relevant genes as well as <italic>LINE1</italic>
 repetitive elements of cord blood mononuclear cells (<italic>n</italic>
 = 261).</p>
<p><bold>Results:</bold>
 No significant difference in promoter methylation levels was shown between ω-3 PUFA–supplemented and control groups for the genes analyzed; however, ω-3 PUFA supplementation was associated with changes in methylation levels in <italic>LINE1</italic>
 repetitive elements (<italic>P</italic>
 = 0.03) in infants of mothers who smoked during pregnancy. Furthermore, an association between the promoter methylation levels of <italic>IFNγ</italic>
 and <italic>IL13</italic>
 was modulated by ω-3 PUFA supplementation (<italic>P</italic>
 = 0.06).</p>
<p><bold>Conclusions:</bold>
 Our results indicate that maternal supplementation with ω-3 PUFA during pregnancy may modulate global methylation levels and the Th1/Th2 balance in infants. Therefore, the epigenetic mechanisms could provide attractive targets for prenatal modulation and prevention of inflammatory disorders and potentially other related diseases in childhood and adulthood.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Clin Nutr</journal-id>
<journal-id journal-id-type="iso-abbrev">Am. J. Clin. Nutr</journal-id>
<journal-id journal-id-type="publisher-id">ajcn</journal-id>
<journal-title-group><journal-title>The American Journal of Clinical Nutrition</journal-title>
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<issn pub-type="ppub">0002-9165</issn>
<issn pub-type="epub">1938-3207</issn>
<publisher><publisher-name>American Society for Nutrition</publisher-name>
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<article-meta><article-id pub-id-type="pmid">23761484</article-id>
<article-id pub-id-type="pmc">3712555</article-id>
<article-id pub-id-type="publisher-id">052241</article-id>
<article-id pub-id-type="doi">10.3945/ajcn.112.052241</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Dietary Supplements</subject>
</subj-group>
</article-categories>
<title-group><article-title>Modulation of DNA methylation states and infant immune system by dietary supplementation with ω-3 PUFA during pregnancy in an intervention study<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="author-notes" rid="fn1"><sup>2</sup>
</xref>
<xref ref-type="author-notes" rid="fn2"><sup>3</sup>
</xref>
<xref ref-type="author-notes" rid="fn3"><sup>4</sup>
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<xref ref-type="corresp" rid="cor1"><sup>5</sup>
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<contrib-group><contrib contrib-type="author"><name><surname>Lee</surname>
<given-names>Ho-Sun</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Barraza-Villarreal</surname>
<given-names>Albino</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Hernandez-Vargas</surname>
<given-names>Hector</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Sly</surname>
<given-names>Peter D</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Biessy</surname>
<given-names>Carine</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Ramakrishnan</surname>
<given-names>Usha</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Romieu</surname>
<given-names>Isabelle</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Herceg</surname>
<given-names>Zdenko</given-names>
</name>
</contrib>
<aff id="aff1"><label>1</label>
From the International Agency for Research on Cancer, Lyon, France (H-SL, HH-V, CB, IR, and ZH); the Instituto Nacional de Salud Pública, Centro de Investigaciones en Salud Poblacional, Cuernavaca, Morelos, Mexico (AB-V and IR); the Queensland Children's Medical Research Institute, Royal Children's Hospital, Herston, Queensland, Australia (PDS); and the Nutrition and Health Sciences and Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA (UR).</aff>
</contrib-group>
<author-notes><fn id="fn1"><label>2</label>
<p>IR and ZH contributed equally to this work.</p>
</fn>
<fn id="fn2"><label>3</label>
<p>The funders had no role in the study design, data collection and analysis, the decision to publish, or preparation of the manuscript.</p>
</fn>
<fn id="fn3"><label>4</label>
<p>Supported by the National Council for Science and Technology, Mexico (grant 14429), and the <italic>Eunice Kennedy Shriver</italic>
 National Institute of Child Health & Human Development of the NIH, United States (award R01HD058818). The work of the International Agency for Research on Cancer (IARC) Epigenetics Group is supported by grants from the National Cancer Institute, NIH, United States; l'Association pour la Recherche sur le Cancer, France; la Ligue Nationale Contre le Cancer, France; the Swiss Bridge Award; and the Bill and Melinda Gates Foundation. HSL was supported by a postdoctoral fellowship from the IARC, partially supported by the European Commission FP7 Marie Curie Actions–People–Cofunding of Regional, National and International Programmes.</p>
</fn>
<corresp id="cor1"><label>5</label>
Address correspondence to Z Herceg, Epigenetics Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, F-69008, Lyon, France. E-mail: <email xlink:type="simple">herceg@iarc.fr</email>
; or I Romieu, Nutritional Epidemiology Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, F-69008, Lyon, France. E-mail: romieui@iarc.fr.</corresp>
</author-notes>
<pmc-comment>Fake ppub date generated by PMC from publisher pub-date/@pub-type='epub-ppub' </pmc-comment>
      <pub-date pub-type="ppub"><month>8</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>12</day>
<month>6</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>8</month>
<year>2014</year>
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<pmc-comment> PMC Release delay is 12 months and 0 days and was based on the . </pmc-comment>
      <volume>98</volume>
<issue>2</issue>
<fpage>480</fpage>
<lpage>487</lpage>
<history><date date-type="received"><day>6</day>
<month>10</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>30</day>
<month>4</month>
<year>2013</year>
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<permissions><copyright-statement>© 2013 American Society for Nutrition</copyright-statement>
<copyright-year>2013</copyright-year>
</permissions>
<abstract><p><bold>Background:</bold>
 Early-life exposures to tobacco smoke and some dietary factors have been identified to induce epigenetic changes in genes involved in allergy and asthma development. Omega-3 (n−3) polyunsaturated fatty acid (PUFA) intake during pregnancy could modulate key cytokines and T helper (Th) cell maturation; however, little is known about the mechanism by which ω-3 PUFA could have a beneficial effect in preventing inflammatory disorders.</p>
<p><bold>Objective:</bold>
 We sought to test whether prenatal dietary supplementation with ω-3 PUFA during pregnancy may modulate epigenetic states in the infant immune system.</p>
<p><bold>Design:</bold>
 This study was based on a randomized intervention trial conducted in Mexican pregnant women supplemented daily with 400 mg docosahexaenoic acid (DHA) or a placebo from 18 to 22 wk of gestation to parturition. We applied quantitative profiling of DNA methylation states in Th1, Th2, Th17, and regulatory T–relevant genes as well as <italic>LINE1</italic>
 repetitive elements of cord blood mononuclear cells (<italic>n</italic>
 = 261).</p>
<p><bold>Results:</bold>
 No significant difference in promoter methylation levels was shown between ω-3 PUFA–supplemented and control groups for the genes analyzed; however, ω-3 PUFA supplementation was associated with changes in methylation levels in <italic>LINE1</italic>
 repetitive elements (<italic>P</italic>
 = 0.03) in infants of mothers who smoked during pregnancy. Furthermore, an association between the promoter methylation levels of <italic>IFNγ</italic>
 and <italic>IL13</italic>
 was modulated by ω-3 PUFA supplementation (<italic>P</italic>
 = 0.06).</p>
<p><bold>Conclusions:</bold>
 Our results indicate that maternal supplementation with ω-3 PUFA during pregnancy may modulate global methylation levels and the Th1/Th2 balance in infants. Therefore, the epigenetic mechanisms could provide attractive targets for prenatal modulation and prevention of inflammatory disorders and potentially other related diseases in childhood and adulthood.</p>
</abstract>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Barraza Villarreal, Albino" sort="Barraza Villarreal, Albino" uniqKey="Barraza Villarreal A" first="Albino" last="Barraza-Villarreal">Albino Barraza-Villarreal</name>
<name sortKey="Biessy, Carine" sort="Biessy, Carine" uniqKey="Biessy C" first="Carine" last="Biessy">Carine Biessy</name>
<name sortKey="Herceg, Zdenko" sort="Herceg, Zdenko" uniqKey="Herceg Z" first="Zdenko" last="Herceg">Zdenko Herceg</name>
<name sortKey="Hernandez Vargas, Hector" sort="Hernandez Vargas, Hector" uniqKey="Hernandez Vargas H" first="Hector" last="Hernandez-Vargas">Hector Hernandez-Vargas</name>
<name sortKey="Lee, Ho Sun" sort="Lee, Ho Sun" uniqKey="Lee H" first="Ho-Sun" last="Lee">Ho-Sun Lee</name>
<name sortKey="Ramakrishnan, Usha" sort="Ramakrishnan, Usha" uniqKey="Ramakrishnan U" first="Usha" last="Ramakrishnan">Usha Ramakrishnan</name>
<name sortKey="Romieu, Isabelle" sort="Romieu, Isabelle" uniqKey="Romieu I" first="Isabelle" last="Romieu">Isabelle Romieu</name>
<name sortKey="Sly, Peter D" sort="Sly, Peter D" uniqKey="Sly P" first="Peter D" last="Sly">Peter D. Sly</name>
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Modulation of DNA methylation states and infant immune system by dietary supplementation with ω-3 PUFA during pregnancy in an intervention study12345

Modulation of DNA methylation states and infant immune system by dietary supplementation with ω-3 PUFA during pregnancy in an intervention study12345

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