Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming

Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have n...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Neurochemistry international 2019-06, Vol.126, p.109-117
Hauptverfasser: Maldonado-Ruiz, Roger, Garza-Ocañas, Lourdes, Camacho, Alberto
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 117
container_issue
container_start_page 109
container_title Neurochemistry international
container_volume 126
creator Maldonado-Ruiz, Roger
Garza-Ocañas, Lourdes
Camacho, Alberto
description Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have not been fully clarified. Maternal immune activation (MIA) during pregnancy have been proposed as a potential etiological cause leading to aberrant synaptic pruning and microglia-mediated neurogenesis impairment. Several clinical studies suggest that pro-inflammatory profile during maternal obesity associates with a higher risk of having a child with autism. In this context, the effect of maternal programing by high fat diet overconsumption during pregnancy sets a pro-inflammatory profile partly dependent on an epigenetic program of immunity which promotes brain micro and macrostructural abnormalities in the offspring that might last through adulthood accompanied by phenotypic changes in ASD subjects. Of note, maternal programming of inflammation during development seems to integrate the CNS and peripheral immune system cross-talk which arrays central inflammatory domains coordinating ASD behavior. In this review, we discuss basic and clinical studies regarding the effects of obesity-induced MIA on peripheral immune cells and microglia priming and their relationship with brain structural alterations in ASD models. Also, we show supportive evidence stating the role of maternal programming on epigenetic gene activation in immune cells of ASD subjects. We suggest that maternal programming by hypercaloric diets during development sets a central and peripheral immune cross-talk which potentially might modulate brain macro and microstructural defects leading to autism susceptibility. •Maternal programming by hypercaloric diets leads to central and peripheral immune system activation.•Central and peripheral immune cross-talk modulates autism susceptibility.•Microglia activation during maternal programming promotes brain structural and synaptic defects.
doi_str_mv 10.1016/j.neuint.2019.03.009
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2193622524</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0197018618306569</els_id><sourcerecordid>2193622524</sourcerecordid><originalsourceid>FETCH-LOGICAL-c362t-b038c01222cedcc1ed6a69ab6f97dd641f9f3676e61d1f3c59ea6a11a3d04ae03</originalsourceid><addsrcrecordid>eNp9kE1rHSEUhqU0NDdp_0Eps-xmJked64ybQAltEwhkk67Fq2eCl1Fv_Qjk38fLTbPsSsHnPa_nIeQrhYECFVf7IWB1oQwMqByADwDyA9nQeWK9nLbjR7JpD1MPdBbn5CLnPQBMErafyDmHeQYYxYb4u7Cs2ntdYnrpbPTahdz5aOuqC3a6Fpd9lw9oSqq-sy7HZDF1uWaDh-J2bnWlBWty4alrYzAFvXahluSKi8f7IcWn1Coa8JmcLXrN-OXtvCR_fv18vLnt7x9-3938uO8NF6z0O-CzAcoYM2iNoWiFFlLvxCIna8VIF7lwMQkU1NKFm61ELTSlmlsYNQK_JN9Pc1v334q5KO_af9dVB4w1K0ZlK2JbNjZ0PKEmxZwTLuqQnNfpRVFQR9Fqr06i1VG0Aq6a6Bb79tZQdx7te-if2QZcnwBsez47TCobh6Et5FKTqWx0_294BdjIlVo</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2193622524</pqid></control><display><type>article</type><title>Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming</title><source>MEDLINE</source><source>ScienceDirect Freedom Collection (Elsevier)</source><creator>Maldonado-Ruiz, Roger ; Garza-Ocañas, Lourdes ; Camacho, Alberto</creator><creatorcontrib>Maldonado-Ruiz, Roger ; Garza-Ocañas, Lourdes ; Camacho, Alberto</creatorcontrib><description>Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have not been fully clarified. Maternal immune activation (MIA) during pregnancy have been proposed as a potential etiological cause leading to aberrant synaptic pruning and microglia-mediated neurogenesis impairment. Several clinical studies suggest that pro-inflammatory profile during maternal obesity associates with a higher risk of having a child with autism. In this context, the effect of maternal programing by high fat diet overconsumption during pregnancy sets a pro-inflammatory profile partly dependent on an epigenetic program of immunity which promotes brain micro and macrostructural abnormalities in the offspring that might last through adulthood accompanied by phenotypic changes in ASD subjects. Of note, maternal programming of inflammation during development seems to integrate the CNS and peripheral immune system cross-talk which arrays central inflammatory domains coordinating ASD behavior. In this review, we discuss basic and clinical studies regarding the effects of obesity-induced MIA on peripheral immune cells and microglia priming and their relationship with brain structural alterations in ASD models. Also, we show supportive evidence stating the role of maternal programming on epigenetic gene activation in immune cells of ASD subjects. We suggest that maternal programming by hypercaloric diets during development sets a central and peripheral immune cross-talk which potentially might modulate brain macro and microstructural defects leading to autism susceptibility. •Maternal programming by hypercaloric diets leads to central and peripheral immune system activation.•Central and peripheral immune cross-talk modulates autism susceptibility.•Microglia activation during maternal programming promotes brain structural and synaptic defects.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/j.neuint.2019.03.009</identifier><identifier>PMID: 30880046</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Animals ; Autism spectrum disorder ; Autism Spectrum Disorder - chemically induced ; Autism Spectrum Disorder - immunology ; Autism Spectrum Disorder - metabolism ; Diet, High-Fat - adverse effects ; Disease Susceptibility - chemically induced ; Disease Susceptibility - immunology ; Disease Susceptibility - metabolism ; Epigenesis, Genetic - physiology ; Female ; Humans ; Inflammation ; Inflammation Mediators - immunology ; Inflammation Mediators - metabolism ; Maternal Health ; Maternal obesity ; Maternal programming ; Obesity - complications ; Obesity - immunology ; Obesity - metabolism ; Overnutrition - complications ; Overnutrition - immunology ; Overnutrition - metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects - chemically induced ; Prenatal Exposure Delayed Effects - immunology ; Prenatal Exposure Delayed Effects - metabolism</subject><ispartof>Neurochemistry international, 2019-06, Vol.126, p.109-117</ispartof><rights>2019</rights><rights>Copyright © 2019. Published by Elsevier Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-b038c01222cedcc1ed6a69ab6f97dd641f9f3676e61d1f3c59ea6a11a3d04ae03</citedby><cites>FETCH-LOGICAL-c362t-b038c01222cedcc1ed6a69ab6f97dd641f9f3676e61d1f3c59ea6a11a3d04ae03</cites><orcidid>0000-0002-2093-0219</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuint.2019.03.009$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30880046$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Maldonado-Ruiz, Roger</creatorcontrib><creatorcontrib>Garza-Ocañas, Lourdes</creatorcontrib><creatorcontrib>Camacho, Alberto</creatorcontrib><title>Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have not been fully clarified. Maternal immune activation (MIA) during pregnancy have been proposed as a potential etiological cause leading to aberrant synaptic pruning and microglia-mediated neurogenesis impairment. Several clinical studies suggest that pro-inflammatory profile during maternal obesity associates with a higher risk of having a child with autism. In this context, the effect of maternal programing by high fat diet overconsumption during pregnancy sets a pro-inflammatory profile partly dependent on an epigenetic program of immunity which promotes brain micro and macrostructural abnormalities in the offspring that might last through adulthood accompanied by phenotypic changes in ASD subjects. Of note, maternal programming of inflammation during development seems to integrate the CNS and peripheral immune system cross-talk which arrays central inflammatory domains coordinating ASD behavior. In this review, we discuss basic and clinical studies regarding the effects of obesity-induced MIA on peripheral immune cells and microglia priming and their relationship with brain structural alterations in ASD models. Also, we show supportive evidence stating the role of maternal programming on epigenetic gene activation in immune cells of ASD subjects. We suggest that maternal programming by hypercaloric diets during development sets a central and peripheral immune cross-talk which potentially might modulate brain macro and microstructural defects leading to autism susceptibility. •Maternal programming by hypercaloric diets leads to central and peripheral immune system activation.•Central and peripheral immune cross-talk modulates autism susceptibility.•Microglia activation during maternal programming promotes brain structural and synaptic defects.</description><subject>Animals</subject><subject>Autism spectrum disorder</subject><subject>Autism Spectrum Disorder - chemically induced</subject><subject>Autism Spectrum Disorder - immunology</subject><subject>Autism Spectrum Disorder - metabolism</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Disease Susceptibility - chemically induced</subject><subject>Disease Susceptibility - immunology</subject><subject>Disease Susceptibility - metabolism</subject><subject>Epigenesis, Genetic - physiology</subject><subject>Female</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation Mediators - immunology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Maternal Health</subject><subject>Maternal obesity</subject><subject>Maternal programming</subject><subject>Obesity - complications</subject><subject>Obesity - immunology</subject><subject>Obesity - metabolism</subject><subject>Overnutrition - complications</subject><subject>Overnutrition - immunology</subject><subject>Overnutrition - metabolism</subject><subject>Pregnancy</subject><subject>Prenatal Exposure Delayed Effects - chemically induced</subject><subject>Prenatal Exposure Delayed Effects - immunology</subject><subject>Prenatal Exposure Delayed Effects - metabolism</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rHSEUhqU0NDdp_0Eps-xmJked64ybQAltEwhkk67Fq2eCl1Fv_Qjk38fLTbPsSsHnPa_nIeQrhYECFVf7IWB1oQwMqByADwDyA9nQeWK9nLbjR7JpD1MPdBbn5CLnPQBMErafyDmHeQYYxYb4u7Cs2ntdYnrpbPTahdz5aOuqC3a6Fpd9lw9oSqq-sy7HZDF1uWaDh-J2bnWlBWty4alrYzAFvXahluSKi8f7IcWn1Coa8JmcLXrN-OXtvCR_fv18vLnt7x9-3938uO8NF6z0O-CzAcoYM2iNoWiFFlLvxCIna8VIF7lwMQkU1NKFm61ELTSlmlsYNQK_JN9Pc1v334q5KO_af9dVB4w1K0ZlK2JbNjZ0PKEmxZwTLuqQnNfpRVFQR9Fqr06i1VG0Aq6a6Bb79tZQdx7te-if2QZcnwBsez47TCobh6Et5FKTqWx0_294BdjIlVo</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Maldonado-Ruiz, Roger</creator><creator>Garza-Ocañas, Lourdes</creator><creator>Camacho, Alberto</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2093-0219</orcidid></search><sort><creationdate>201906</creationdate><title>Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming</title><author>Maldonado-Ruiz, Roger ; Garza-Ocañas, Lourdes ; Camacho, Alberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-b038c01222cedcc1ed6a69ab6f97dd641f9f3676e61d1f3c59ea6a11a3d04ae03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Autism spectrum disorder</topic><topic>Autism Spectrum Disorder - chemically induced</topic><topic>Autism Spectrum Disorder - immunology</topic><topic>Autism Spectrum Disorder - metabolism</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Disease Susceptibility - chemically induced</topic><topic>Disease Susceptibility - immunology</topic><topic>Disease Susceptibility - metabolism</topic><topic>Epigenesis, Genetic - physiology</topic><topic>Female</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation Mediators - immunology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Maternal Health</topic><topic>Maternal obesity</topic><topic>Maternal programming</topic><topic>Obesity - complications</topic><topic>Obesity - immunology</topic><topic>Obesity - metabolism</topic><topic>Overnutrition - complications</topic><topic>Overnutrition - immunology</topic><topic>Overnutrition - metabolism</topic><topic>Pregnancy</topic><topic>Prenatal Exposure Delayed Effects - chemically induced</topic><topic>Prenatal Exposure Delayed Effects - immunology</topic><topic>Prenatal Exposure Delayed Effects - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maldonado-Ruiz, Roger</creatorcontrib><creatorcontrib>Garza-Ocañas, Lourdes</creatorcontrib><creatorcontrib>Camacho, Alberto</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maldonado-Ruiz, Roger</au><au>Garza-Ocañas, Lourdes</au><au>Camacho, Alberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>2019-06</date><risdate>2019</risdate><volume>126</volume><spage>109</spage><epage>117</epage><pages>109-117</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><abstract>Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have not been fully clarified. Maternal immune activation (MIA) during pregnancy have been proposed as a potential etiological cause leading to aberrant synaptic pruning and microglia-mediated neurogenesis impairment. Several clinical studies suggest that pro-inflammatory profile during maternal obesity associates with a higher risk of having a child with autism. In this context, the effect of maternal programing by high fat diet overconsumption during pregnancy sets a pro-inflammatory profile partly dependent on an epigenetic program of immunity which promotes brain micro and macrostructural abnormalities in the offspring that might last through adulthood accompanied by phenotypic changes in ASD subjects. Of note, maternal programming of inflammation during development seems to integrate the CNS and peripheral immune system cross-talk which arrays central inflammatory domains coordinating ASD behavior. In this review, we discuss basic and clinical studies regarding the effects of obesity-induced MIA on peripheral immune cells and microglia priming and their relationship with brain structural alterations in ASD models. Also, we show supportive evidence stating the role of maternal programming on epigenetic gene activation in immune cells of ASD subjects. We suggest that maternal programming by hypercaloric diets during development sets a central and peripheral immune cross-talk which potentially might modulate brain macro and microstructural defects leading to autism susceptibility. •Maternal programming by hypercaloric diets leads to central and peripheral immune system activation.•Central and peripheral immune cross-talk modulates autism susceptibility.•Microglia activation during maternal programming promotes brain structural and synaptic defects.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>30880046</pmid><doi>10.1016/j.neuint.2019.03.009</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-2093-0219</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0197-0186
ispartof Neurochemistry international, 2019-06, Vol.126, p.109-117
issn 0197-0186
1872-9754
language eng
recordid cdi_proquest_miscellaneous_2193622524
source MEDLINE; ScienceDirect Freedom Collection (Elsevier)
subjects Animals
Autism spectrum disorder
Autism Spectrum Disorder - chemically induced
Autism Spectrum Disorder - immunology
Autism Spectrum Disorder - metabolism
Diet, High-Fat - adverse effects
Disease Susceptibility - chemically induced
Disease Susceptibility - immunology
Disease Susceptibility - metabolism
Epigenesis, Genetic - physiology
Female
Humans
Inflammation
Inflammation Mediators - immunology
Inflammation Mediators - metabolism
Maternal Health
Maternal obesity
Maternal programming
Obesity - complications
Obesity - immunology
Obesity - metabolism
Overnutrition - complications
Overnutrition - immunology
Overnutrition - metabolism
Pregnancy
Prenatal Exposure Delayed Effects - chemically induced
Prenatal Exposure Delayed Effects - immunology
Prenatal Exposure Delayed Effects - metabolism
title Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T05%3A53%3A36IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inflammatory%20domains%20modulate%20autism%20spectrum%20disorder%20susceptibility%20during%20maternal%20nutritional%20programming&rft.jtitle=Neurochemistry%20international&rft.au=Maldonado-Ruiz,%20Roger&rft.date=2019-06&rft.volume=126&rft.spage=109&rft.epage=117&rft.pages=109-117&rft.issn=0197-0186&rft.eissn=1872-9754&rft_id=info:doi/10.1016/j.neuint.2019.03.009&rft_dat=%3Cproquest_cross%3E2193622524%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2193622524&rft_id=info:pmid/30880046&rft_els_id=S0197018618306569&rfr_iscdi=true