Inflammatory Biomarkers are Correlated with Some Forms of Regressive Autism Spectrum Disorder
: Several studies have tried to investigate the role of inflammatory biomarkers in Autism Spectrum Disorder (ASD), and their correlations with clinical phenotypes. Despite the growing research in this topic, existing data are mostly contradictory. : Eighty-five ASD preschoolers were assessed for dev...
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| Veröffentlicht in: | Brain sciences 2019-12, Vol.9 (12), p.366 |
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| creator | Prosperi, Margherita Guiducci, Letizia Peroni, Diego G Narducci, Chiara Gaggini, Melania Calderoni, Sara Tancredi, Raffaella Morales, Maria Aurora Gastaldelli, Amalia Muratori, Filippo Santocchi, Elisa |
| description | : Several studies have tried to investigate the role of inflammatory biomarkers in Autism Spectrum Disorder (ASD), and their correlations with clinical phenotypes. Despite the growing research in this topic, existing data are mostly contradictory.
: Eighty-five ASD preschoolers were assessed for developmental level, adaptive functioning, gastrointestinal (GI), socio-communicative and psychopathological symptoms. Plasma levels of leptin, resistin, plasminogen activator inhibitor-1 (PAI-1), macrophage chemoattractant protein-1 (CCL2), tumor necrosis factor-alfa (TNF-α), and interleukin-6 (IL-6) were correlated with clinical scores and were compared among different ASD subgroups according to the presence or absence of: (i) GI symptoms, (ii) regressive onset of autism.
: Proinflammatory cytokines (TNF-α, IL-6 and CCL2) were lower than those reported in previous studies in children with systemic inflammatory conditions. GI symptoms were not correlated with levels of inflammatory biomarkers except for resistin that was lower in ASD-GI children (
= 0.032). Resistin and PAI-1 levels were significantly higher in the group with "regression plus a developmental delay" onset (Reg+DD group) compared to groups without regression or with regression without a developmental delay (
< 0.01 for all).
: Our results did not highlight the presence of any systemic inflammatory state in ASD subjects neither disentangling children with/without GI symptoms. The Reg + DD group significantly differed from others in some plasmatic values, but these differences failed to discriminate the subgroups as possible distinct ASD endo-phenotypes. |
| doi_str_mv | 10.3390/brainsci9120366 |
| format | Article |
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: Eighty-five ASD preschoolers were assessed for developmental level, adaptive functioning, gastrointestinal (GI), socio-communicative and psychopathological symptoms. Plasma levels of leptin, resistin, plasminogen activator inhibitor-1 (PAI-1), macrophage chemoattractant protein-1 (CCL2), tumor necrosis factor-alfa (TNF-α), and interleukin-6 (IL-6) were correlated with clinical scores and were compared among different ASD subgroups according to the presence or absence of: (i) GI symptoms, (ii) regressive onset of autism.
: Proinflammatory cytokines (TNF-α, IL-6 and CCL2) were lower than those reported in previous studies in children with systemic inflammatory conditions. GI symptoms were not correlated with levels of inflammatory biomarkers except for resistin that was lower in ASD-GI children (
= 0.032). Resistin and PAI-1 levels were significantly higher in the group with "regression plus a developmental delay" onset (Reg+DD group) compared to groups without regression or with regression without a developmental delay (
< 0.01 for all).
: Our results did not highlight the presence of any systemic inflammatory state in ASD subjects neither disentangling children with/without GI symptoms. The Reg + DD group significantly differed from others in some plasmatic values, but these differences failed to discriminate the subgroups as possible distinct ASD endo-phenotypes.</description><identifier>ISSN: 2076-3425</identifier><identifier>EISSN: 2076-3425</identifier><identifier>DOI: 10.3390/brainsci9120366</identifier><identifier>PMID: 31835709</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Autism ; Biomarkers ; Children ; Communication ; Cytokines ; Diabetes ; Disease ; Inflammation ; Insulin resistance ; Interleukin 6 ; Leptin ; Macrophages ; Mental disorders ; Metabolism ; Monocyte chemoattractant protein 1 ; Pathogenesis ; Phenotypes ; Plasma levels ; Plasminogen activator inhibitors ; Preschool children ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Brain sciences, 2019-12, Vol.9 (12), p.366</ispartof><rights>2019 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 (http://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><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-1def0d133d993f2c9549eb48a3f6037a121485eb9602e7572638552b6931b2163</citedby><cites>FETCH-LOGICAL-c421t-1def0d133d993f2c9549eb48a3f6037a121485eb9602e7572638552b6931b2163</cites><orcidid>0000-0002-0234-1373 ; 0000-0003-2594-1651 ; 0000-0003-3330-3238 ; 0000-0002-9917-788X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6955787/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6955787/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31835709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prosperi, Margherita</creatorcontrib><creatorcontrib>Guiducci, Letizia</creatorcontrib><creatorcontrib>Peroni, Diego G</creatorcontrib><creatorcontrib>Narducci, Chiara</creatorcontrib><creatorcontrib>Gaggini, Melania</creatorcontrib><creatorcontrib>Calderoni, Sara</creatorcontrib><creatorcontrib>Tancredi, Raffaella</creatorcontrib><creatorcontrib>Morales, Maria Aurora</creatorcontrib><creatorcontrib>Gastaldelli, Amalia</creatorcontrib><creatorcontrib>Muratori, Filippo</creatorcontrib><creatorcontrib>Santocchi, Elisa</creatorcontrib><title>Inflammatory Biomarkers are Correlated with Some Forms of Regressive Autism Spectrum Disorder</title><title>Brain sciences</title><addtitle>Brain Sci</addtitle><description>: Several studies have tried to investigate the role of inflammatory biomarkers in Autism Spectrum Disorder (ASD), and their correlations with clinical phenotypes. Despite the growing research in this topic, existing data are mostly contradictory.
: Eighty-five ASD preschoolers were assessed for developmental level, adaptive functioning, gastrointestinal (GI), socio-communicative and psychopathological symptoms. Plasma levels of leptin, resistin, plasminogen activator inhibitor-1 (PAI-1), macrophage chemoattractant protein-1 (CCL2), tumor necrosis factor-alfa (TNF-α), and interleukin-6 (IL-6) were correlated with clinical scores and were compared among different ASD subgroups according to the presence or absence of: (i) GI symptoms, (ii) regressive onset of autism.
: Proinflammatory cytokines (TNF-α, IL-6 and CCL2) were lower than those reported in previous studies in children with systemic inflammatory conditions. GI symptoms were not correlated with levels of inflammatory biomarkers except for resistin that was lower in ASD-GI children (
= 0.032). Resistin and PAI-1 levels were significantly higher in the group with "regression plus a developmental delay" onset (Reg+DD group) compared to groups without regression or with regression without a developmental delay (
< 0.01 for all).
: Our results did not highlight the presence of any systemic inflammatory state in ASD subjects neither disentangling children with/without GI symptoms. The Reg + DD group significantly differed from others in some plasmatic values, but these differences failed to discriminate the subgroups as possible distinct ASD endo-phenotypes.</description><subject>Autism</subject><subject>Biomarkers</subject><subject>Children</subject><subject>Communication</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Disease</subject><subject>Inflammation</subject><subject>Insulin resistance</subject><subject>Interleukin 6</subject><subject>Leptin</subject><subject>Macrophages</subject><subject>Mental disorders</subject><subject>Metabolism</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Pathogenesis</subject><subject>Phenotypes</subject><subject>Plasma levels</subject><subject>Plasminogen activator inhibitors</subject><subject>Preschool children</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>2076-3425</issn><issn>2076-3425</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc9LHTEQx0OpVFHPvZVAL708TTKb7OZSsK8-FR4I2h5LyO7Oauxm8zrZtfjfu-IP1LnMwHzmy3z5MvZZigMAKw5r8mHITbBSCTDmA9tRojQLKJT--GreZvs534i5KiFAi09sG2QFuhR2h_05G7rex-jHRHf8R0jR01-kzD0hXyYi7P2ILf8fxmt-mSLyVaKYeer4BV4R5hxukR9NY8iRX26wGWmK_GfIiVqkPbbV-T7j_lPfZb9Xx7-Wp4v1-cnZ8mi9aAolx4VssROtBGithU41VhcW66Ly0BkBpZdKFpXG2hqhsNSlMlBprWpjQdZKGthl3x91N1MdsW1wGMn3bkNhtnPnkg_u7WYI1-4q3TpjtS6rchb49iRA6d-EeXQx5Ab73g-YpuwUgLHWzt_O6Nd36E2aaJjtOaVBS1tpVczU4SPVUMqZsHt5Rgr3kJ57l9588eW1hxf-OSu4B-NVlz8</recordid><startdate>20191211</startdate><enddate>20191211</enddate><creator>Prosperi, Margherita</creator><creator>Guiducci, Letizia</creator><creator>Peroni, Diego G</creator><creator>Narducci, Chiara</creator><creator>Gaggini, Melania</creator><creator>Calderoni, Sara</creator><creator>Tancredi, Raffaella</creator><creator>Morales, Maria Aurora</creator><creator>Gastaldelli, Amalia</creator><creator>Muratori, Filippo</creator><creator>Santocchi, Elisa</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PKEHL</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0234-1373</orcidid><orcidid>https://orcid.org/0000-0003-2594-1651</orcidid><orcidid>https://orcid.org/0000-0003-3330-3238</orcidid><orcidid>https://orcid.org/0000-0002-9917-788X</orcidid></search><sort><creationdate>20191211</creationdate><title>Inflammatory Biomarkers are Correlated with Some Forms of Regressive Autism Spectrum Disorder</title><author>Prosperi, Margherita ; 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Despite the growing research in this topic, existing data are mostly contradictory.
: Eighty-five ASD preschoolers were assessed for developmental level, adaptive functioning, gastrointestinal (GI), socio-communicative and psychopathological symptoms. Plasma levels of leptin, resistin, plasminogen activator inhibitor-1 (PAI-1), macrophage chemoattractant protein-1 (CCL2), tumor necrosis factor-alfa (TNF-α), and interleukin-6 (IL-6) were correlated with clinical scores and were compared among different ASD subgroups according to the presence or absence of: (i) GI symptoms, (ii) regressive onset of autism.
: Proinflammatory cytokines (TNF-α, IL-6 and CCL2) were lower than those reported in previous studies in children with systemic inflammatory conditions. GI symptoms were not correlated with levels of inflammatory biomarkers except for resistin that was lower in ASD-GI children (
= 0.032). Resistin and PAI-1 levels were significantly higher in the group with "regression plus a developmental delay" onset (Reg+DD group) compared to groups without regression or with regression without a developmental delay (
< 0.01 for all).
: Our results did not highlight the presence of any systemic inflammatory state in ASD subjects neither disentangling children with/without GI symptoms. The Reg + DD group significantly differed from others in some plasmatic values, but these differences failed to discriminate the subgroups as possible distinct ASD endo-phenotypes.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31835709</pmid><doi>10.3390/brainsci9120366</doi><orcidid>https://orcid.org/0000-0002-0234-1373</orcidid><orcidid>https://orcid.org/0000-0003-2594-1651</orcidid><orcidid>https://orcid.org/0000-0003-3330-3238</orcidid><orcidid>https://orcid.org/0000-0002-9917-788X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Autism Biomarkers Children Communication Cytokines Diabetes Disease Inflammation Insulin resistance Interleukin 6 Leptin Macrophages Mental disorders Metabolism Monocyte chemoattractant protein 1 Pathogenesis Phenotypes Plasma levels Plasminogen activator inhibitors Preschool children Tumor necrosis factor-TNF Tumor necrosis factor-α |
| title | Inflammatory Biomarkers are Correlated with Some Forms of Regressive Autism Spectrum Disorder |
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