3 recherche sur le mot-clé 'Immune response'

Maternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study / Heather E. VOLK in Journal of Neurodevelopmental Disorders, 12 (2020)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 12 (2020) Titre : Maternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study Type de document : texte imprimé Auteurs : Heather E. VOLK, Auteur ; Bo PARK, Auteur ; Calliope HOLLINGUE, Auteur ; Karen L. JONES, Auteur ; Paul ASHWOOD, Auteur ; Gayle C. WINDHAM, Auteur ; Fred LURMAN, Auteur ; Stacey E. ALEXEEFF, Auteur ; Martin KHARRAZI, Auteur ; Michelle PEARL, Auteur ; Judy VAN DE WATER, Auteur ; Lisa A. CROEN, Auteur Langues : Anglais (eng) Mots-clés : Air Pollution/adverse effects  Autistic Disorder  Biomarkers  Case-Control Studies  Child  Female  Humans  Immunity  Male  Pregnancy/immunology  Prenatal Exposure Delayed Effects  United States  Air pollution  Autism spectrum disorder  Immune response  Intellectual disability  Prenatal exposure  declare. Index. décimale : PER Périodiques Résumé : BACKGROUND: Perinatal exposure to air pollution and immune system dysregulation are two factors consistently associated with autism spectrum disorders (ASD) and other neurodevelopmental outcomes. However, little is known about how air pollution may influence maternal immune function during pregnancy. OBJECTIVES: To assess the relationship between mid-gestational circulating levels of maternal cytokines/chemokines and previous month air pollution exposure across neurodevelopmental groups, and to assess whether cytokines/chemokines mediate the relationship between air pollution exposures and risk of ASD and/or intellectual disability (ID) in the Early Markers for Autism (EMA) study. METHODS: EMA is a population-based, nested case-control study which linked archived maternal serum samples collected during weeks 15-19 of gestation for routine prenatal screening, birth records, and Department of Developmental Services (DDS) records. Children receiving DDS services for ASD without intellectual disability (ASD without ID; n = 199), ASD with ID (ASD with ID; n = 180), ID without ASD (ID; n = 164), and children from the general population (GP; n = 414) with no DDS services were included in this analysis. Serum samples were quantified for 22 cytokines/chemokines using Luminex multiplex analysis technology. Air pollution exposure for the month prior to maternal serum collection was assigned based on the Environmental Protection Agency's Air Quality System data using the maternal residential address reported during the prenatal screening visit. RESULTS: Previous month air pollution exposure and mid-gestational maternal cytokine and chemokine levels were significantly correlated, though weak in magnitude (ranging from - 0.16 to 0.13). Ten pairs of mid-pregnancy immune markers and previous month air pollutants were significantly associated within one of the child neurodevelopmental groups, adjusted for covariates (p < 0.001). Mid-pregnancy air pollution was not associated with any neurodevelopmental outcome. IL-6 remained associated with ASD with ID even after adjusting for air pollution exposure. CONCLUSION: This study suggests that maternal immune activation is associated with risk for neurodevelopmental disorders. Furthermore, that prenatal air pollution exposure is associated with small, but perhaps biologically relevant, effects on maternal immune system function during pregnancy. Additional studies are needed to better evaluate how prenatal exposure to air pollution affects the trajectory of maternal immune activation during pregnancy, if windows of heightened susceptibility can be identified, and how these factors influence neurodevelopment of the offspring. En ligne : https://dx.doi.org/10.1186/s11689-020-09343-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573 [article] Maternal immune response and air pollution exposure during pregnancy: insights from the Early Markers for Autism (EMA) study [texte imprimé] / Heather E. VOLK, Auteur ; Bo PARK, Auteur ; Calliope HOLLINGUE, Auteur ; Karen L. JONES, Auteur ; Paul ASHWOOD, Auteur ; Gayle C. WINDHAM, Auteur ; Fred LURMAN, Auteur ; Stacey E. ALEXEEFF, Auteur ; Martin KHARRAZI, Auteur ; Michelle PEARL, Auteur ; Judy VAN DE WATER, Auteur ; Lisa A. CROEN, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 12 (2020) Mots-clés : Air Pollution/adverse effects  Autistic Disorder  Biomarkers  Case-Control Studies  Child  Female  Humans  Immunity  Male  Pregnancy/immunology  Prenatal Exposure Delayed Effects  United States  Air pollution  Autism spectrum disorder  Immune response  Intellectual disability  Prenatal exposure  declare. Index. décimale : PER Périodiques Résumé : BACKGROUND: Perinatal exposure to air pollution and immune system dysregulation are two factors consistently associated with autism spectrum disorders (ASD) and other neurodevelopmental outcomes. However, little is known about how air pollution may influence maternal immune function during pregnancy. OBJECTIVES: To assess the relationship between mid-gestational circulating levels of maternal cytokines/chemokines and previous month air pollution exposure across neurodevelopmental groups, and to assess whether cytokines/chemokines mediate the relationship between air pollution exposures and risk of ASD and/or intellectual disability (ID) in the Early Markers for Autism (EMA) study. METHODS: EMA is a population-based, nested case-control study which linked archived maternal serum samples collected during weeks 15-19 of gestation for routine prenatal screening, birth records, and Department of Developmental Services (DDS) records. Children receiving DDS services for ASD without intellectual disability (ASD without ID; n = 199), ASD with ID (ASD with ID; n = 180), ID without ASD (ID; n = 164), and children from the general population (GP; n = 414) with no DDS services were included in this analysis. Serum samples were quantified for 22 cytokines/chemokines using Luminex multiplex analysis technology. Air pollution exposure for the month prior to maternal serum collection was assigned based on the Environmental Protection Agency's Air Quality System data using the maternal residential address reported during the prenatal screening visit. RESULTS: Previous month air pollution exposure and mid-gestational maternal cytokine and chemokine levels were significantly correlated, though weak in magnitude (ranging from - 0.16 to 0.13). Ten pairs of mid-pregnancy immune markers and previous month air pollutants were significantly associated within one of the child neurodevelopmental groups, adjusted for covariates (p < 0.001). Mid-pregnancy air pollution was not associated with any neurodevelopmental outcome. IL-6 remained associated with ASD with ID even after adjusting for air pollution exposure. CONCLUSION: This study suggests that maternal immune activation is associated with risk for neurodevelopmental disorders. Furthermore, that prenatal air pollution exposure is associated with small, but perhaps biologically relevant, effects on maternal immune system function during pregnancy. Additional studies are needed to better evaluate how prenatal exposure to air pollution affects the trajectory of maternal immune activation during pregnancy, if windows of heightened susceptibility can be identified, and how these factors influence neurodevelopment of the offspring. En ligne : https://dx.doi.org/10.1186/s11689-020-09343-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=573

Common and rare variant analyses implicate late-infancy cerebellar development and immune genes in ADHD / Yuanxin ZHONG in Journal of Neurodevelopmental Disorders, 17 (2025)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 17 (2025) Titre : Common and rare variant analyses implicate late-infancy cerebellar development and immune genes in ADHD Type de document : texte imprimé Auteurs : Yuanxin ZHONG, Auteur ; Larry W. BAUM, Auteur ; Justin D. TUBBS, Auteur ; Rui YE, Auteur ; Lu Hua CHEN, Auteur ; Tian WU, Auteur ; Se-fong HUNG, Auteur ; Chun-pan TANG, Auteur ; Ting-pong HO, Auteur ; Robert MOYZIS, Auteur ; James SWANSON, Auteur ; Chi-chiu LEE, Auteur ; Pak C. SHAM, Auteur ; Patrick W.L. LEUNG, Auteur Langues : Anglais (eng) Mots-clés : Humans  Attention Deficit Disorder with  Hyperactivity/genetics/immunology/physiopathology  Cerebellum/growth & development/diagnostic imaging/physiopathology  Male  Female  Genome-Wide Association Study  Genetic Predisposition to Disease  Child  Magnetic Resonance Imaging  Hong Kong  Polymorphism, Single Nucleotide  Infant  Adhd  Cerebellum  Common variant  Immune response  Late-infancy  Low-frequency / rare variant  University of Hong Kong-New Territories East Cluster, the Hospital Authority  Kowloon Central and Kowloon West Cluster Clinical Research Ethics Committee  provided ethical approval for this study, which complies with the most recent  Declaration of Helsinki. All participants provided informed consent for the  current study. Consent for publication: Not applicable. Competing interests: The  authors declare no competing interests. Index. décimale : PER Périodiques Résumé : OBJECTIVE: Attention-deficit hyperactivity disorder (ADHD) is a common neuropsychiatric disorder with a significant genetic component. The latest genome-wide association study (GWAS) meta-analysis of ADHD identified 27 whole-genome significant risk loci in the European population. However, genetic risk factors for ADHD are less well-characterized in the Asian population, especially for low-frequency / rare variants. METHODS: In this study, we aimed to investigate the contributions of both common and low-frequency / rare variants to ADHD in a Hong Kong sample. Our sample comprised 279 cases and 432 controls who underwent genotyping using the Illumina Infinium Global Screening Array. We employed various analytical methods at different levels, while also leveraging multi-omics data and large-scale summary statistics to comprehensively analyze the genetic basis of ADHD. RESULTS: We identified 41 potential genomic risk loci with a suggestive association (p < 1e(-4)), pointing to 111 candidate risk genes, which were enriched for genes differentially expressed during late infancy brain development. Furthermore, tissue enrichment analysis implicated the involvement of the cerebellum. At the polygenic level, we also discovered a strong genetic correlation with resting-state functional MRI connectivity of the cerebellum involved in the attention/central executive and subcortical-cerebellum networks. In addition, an accumulation of ADHD common-variant risks found in European ancestry samples was found to be significantly associated with ADHD in the current study. In low-frequency / rare variant analyses, we discovered the correlations between ADHD and collapsing effects of rare damaging variants in TEP1, MTMR10, DBH, TBCC, and ANO1. Based on biological and functional profiles of the potential risk genes and gene sets, both common and low-frequency / rare variant analyses demonstrated that ADHD genetic risk was associated with immune processes. CONCLUSIONS: These findings re-validate the abnormal development of the neural system in ADHD and extend the existing neuro-dysfunction hypothesis to a multi-system perspective. The current study identified convergent risk factors from common and low-frequency / rare variants, which implicates vulnerability in late-infancy brain development, affecting especially the cerebellum, and the involvement of immune processes. En ligne : https://dx.doi.org/10.1186/s11689-025-09626-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 [article] Common and rare variant analyses implicate late-infancy cerebellar development and immune genes in ADHD [texte imprimé] / Yuanxin ZHONG, Auteur ; Larry W. BAUM, Auteur ; Justin D. TUBBS, Auteur ; Rui YE, Auteur ; Lu Hua CHEN, Auteur ; Tian WU, Auteur ; Se-fong HUNG, Auteur ; Chun-pan TANG, Auteur ; Ting-pong HO, Auteur ; Robert MOYZIS, Auteur ; James SWANSON, Auteur ; Chi-chiu LEE, Auteur ; Pak C. SHAM, Auteur ; Patrick W.L. LEUNG, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 17 (2025) Mots-clés : Humans  Attention Deficit Disorder with  Hyperactivity/genetics/immunology/physiopathology  Cerebellum/growth & development/diagnostic imaging/physiopathology  Male  Female  Genome-Wide Association Study  Genetic Predisposition to Disease  Child  Magnetic Resonance Imaging  Hong Kong  Polymorphism, Single Nucleotide  Infant  Adhd  Cerebellum  Common variant  Immune response  Late-infancy  Low-frequency / rare variant  University of Hong Kong-New Territories East Cluster, the Hospital Authority  Kowloon Central and Kowloon West Cluster Clinical Research Ethics Committee  provided ethical approval for this study, which complies with the most recent  Declaration of Helsinki. All participants provided informed consent for the  current study. Consent for publication: Not applicable. Competing interests: The  authors declare no competing interests. Index. décimale : PER Périodiques Résumé : OBJECTIVE: Attention-deficit hyperactivity disorder (ADHD) is a common neuropsychiatric disorder with a significant genetic component. The latest genome-wide association study (GWAS) meta-analysis of ADHD identified 27 whole-genome significant risk loci in the European population. However, genetic risk factors for ADHD are less well-characterized in the Asian population, especially for low-frequency / rare variants. METHODS: In this study, we aimed to investigate the contributions of both common and low-frequency / rare variants to ADHD in a Hong Kong sample. Our sample comprised 279 cases and 432 controls who underwent genotyping using the Illumina Infinium Global Screening Array. We employed various analytical methods at different levels, while also leveraging multi-omics data and large-scale summary statistics to comprehensively analyze the genetic basis of ADHD. RESULTS: We identified 41 potential genomic risk loci with a suggestive association (p < 1e(-4)), pointing to 111 candidate risk genes, which were enriched for genes differentially expressed during late infancy brain development. Furthermore, tissue enrichment analysis implicated the involvement of the cerebellum. At the polygenic level, we also discovered a strong genetic correlation with resting-state functional MRI connectivity of the cerebellum involved in the attention/central executive and subcortical-cerebellum networks. In addition, an accumulation of ADHD common-variant risks found in European ancestry samples was found to be significantly associated with ADHD in the current study. In low-frequency / rare variant analyses, we discovered the correlations between ADHD and collapsing effects of rare damaging variants in TEP1, MTMR10, DBH, TBCC, and ANO1. Based on biological and functional profiles of the potential risk genes and gene sets, both common and low-frequency / rare variant analyses demonstrated that ADHD genetic risk was associated with immune processes. CONCLUSIONS: These findings re-validate the abnormal development of the neural system in ADHD and extend the existing neuro-dysfunction hypothesis to a multi-system perspective. The current study identified convergent risk factors from common and low-frequency / rare variants, which implicates vulnerability in late-infancy brain development, affecting especially the cerebellum, and the involvement of immune processes. En ligne : https://dx.doi.org/10.1186/s11689-025-09626-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576

A profile and review of findings from the Early Markers for Autism study: unique contributions from a population-based case-control study in California / Kristen LYALL in Molecular Autism, 12 (2021)  

Public ISBD [article]  inMolecular Autism > 12 (2021) . - 24 p. Titre : A profile and review of findings from the Early Markers for Autism study: unique contributions from a population-based case-control study in California Type de document : texte imprimé Auteurs : Kristen LYALL, Auteur ; Jennifer L. AMES, Auteur ; Michelle PEARL, Auteur ; Michela TRAGLIA, Auteur ; Lauren A. WEISS, Auteur ; Gayle C. WINDHAM, Auteur ; Martin KHARRAZI, Auteur ; Cathleen K. YOSHIDA, Auteur ; Robert YOLKEN, Auteur ; Heather E. VOLK, Auteur ; Paul ASHWOOD, Auteur ; Judy VAN DE WATER, Auteur ; Lisa A. CROEN, Auteur Article en page(s) : 24 p. Langues : Anglais (eng) Mots-clés : Adult  Autistic Disorder/blood/epidemiology/immunology  Biomarkers/blood  California/epidemiology  Case-Control Studies  Child  Cytokines/immunology  Endocrine Disruptors  Environmental Exposure  Environmental Pollutants  Female  Humans  Male  Pregnancy/immunology  Thyroid Hormones/blood  Vitamin D/blood  Young Adult  Autism  Early Markers for Autism  Immune response  Risk factors Index. décimale : PER Périodiques Résumé : BACKGROUND: The Early Markers for Autism (EMA) study is a population-based case-control study designed to learn more about early biologic processes involved in ASD. METHODS: Participants were drawn from Southern California births from 2000 to 2003 with archived prenatal and neonatal screening specimens. Across two phases, children with ASD (n = 629) and intellectual disability without ASD (ID, n = 230) were ascertained from the California Department of Developmental Services (DDS), with diagnoses confirmed according to DSM-IV-TR criteria based on expert clinical review of abstracted records. General population controls (GP, n = 599) were randomly sampled from birth certificate files and matched to ASD cases by sex, birth month and year after excluding individuals with DDS records. EMA has published over 20 papers examining immune markers, endogenous hormones, environmental chemicals, and genetic factors in association with ASD and ID. This review summarizes the results across these studies, as well as the EMA study design and future directions. RESULTS: EMA enabled several key contributions to the literature, including the examination of biomarker levels in biospecimens prospectively collected during critical windows of neurodevelopment. Key findings from EMA include demonstration of elevated cytokine and chemokine levels in maternal mid-pregnancy serum samples in association with ASD, as well as aberrations in other immune marker levels; suggestions of increased odds of ASD with prenatal exposure to certain endocrine disrupting chemicals, though not in mixture analyses; and demonstration of maternal and fetal genetic influence on prenatal chemical, and maternal and neonatal immune marker and vitamin D levels. We also observed an overall lack of association with ASD and measured maternal and neonatal vitamin D, mercury, and brain-derived neurotrophic factor (BDNF) levels. LIMITATIONS: Covariate and outcome data were limited to information in Vital Statistics and DDS records. As a study based in Southern California, generalizability for certain environmental exposures may be reduced. CONCLUSIONS: Results across EMA studies support the importance of the prenatal and neonatal periods in ASD etiology, and provide evidence for the role of the maternal immune response during pregnancy. Future directions for EMA, and the field of ASD in general, include interrogation of mechanistic pathways and examination of combined effects of exposures. En ligne : http://dx.doi.org/10.1186/s13229-021-00429-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 [article] A profile and review of findings from the Early Markers for Autism study: unique contributions from a population-based case-control study in California [texte imprimé] / Kristen LYALL, Auteur ; Jennifer L. AMES, Auteur ; Michelle PEARL, Auteur ; Michela TRAGLIA, Auteur ; Lauren A. WEISS, Auteur ; Gayle C. WINDHAM, Auteur ; Martin KHARRAZI, Auteur ; Cathleen K. YOSHIDA, Auteur ; Robert YOLKEN, Auteur ; Heather E. VOLK, Auteur ; Paul ASHWOOD, Auteur ; Judy VAN DE WATER, Auteur ; Lisa A. CROEN, Auteur . - 24 p. Langues : Anglais (eng) in Molecular Autism > 12 (2021) . - 24 p. Mots-clés : Adult  Autistic Disorder/blood/epidemiology/immunology  Biomarkers/blood  California/epidemiology  Case-Control Studies  Child  Cytokines/immunology  Endocrine Disruptors  Environmental Exposure  Environmental Pollutants  Female  Humans  Male  Pregnancy/immunology  Thyroid Hormones/blood  Vitamin D/blood  Young Adult  Autism  Early Markers for Autism  Immune response  Risk factors Index. décimale : PER Périodiques Résumé : BACKGROUND: The Early Markers for Autism (EMA) study is a population-based case-control study designed to learn more about early biologic processes involved in ASD. METHODS: Participants were drawn from Southern California births from 2000 to 2003 with archived prenatal and neonatal screening specimens. Across two phases, children with ASD (n = 629) and intellectual disability without ASD (ID, n = 230) were ascertained from the California Department of Developmental Services (DDS), with diagnoses confirmed according to DSM-IV-TR criteria based on expert clinical review of abstracted records. General population controls (GP, n = 599) were randomly sampled from birth certificate files and matched to ASD cases by sex, birth month and year after excluding individuals with DDS records. EMA has published over 20 papers examining immune markers, endogenous hormones, environmental chemicals, and genetic factors in association with ASD and ID. This review summarizes the results across these studies, as well as the EMA study design and future directions. RESULTS: EMA enabled several key contributions to the literature, including the examination of biomarker levels in biospecimens prospectively collected during critical windows of neurodevelopment. Key findings from EMA include demonstration of elevated cytokine and chemokine levels in maternal mid-pregnancy serum samples in association with ASD, as well as aberrations in other immune marker levels; suggestions of increased odds of ASD with prenatal exposure to certain endocrine disrupting chemicals, though not in mixture analyses; and demonstration of maternal and fetal genetic influence on prenatal chemical, and maternal and neonatal immune marker and vitamin D levels. We also observed an overall lack of association with ASD and measured maternal and neonatal vitamin D, mercury, and brain-derived neurotrophic factor (BDNF) levels. LIMITATIONS: Covariate and outcome data were limited to information in Vital Statistics and DDS records. As a study based in Southern California, generalizability for certain environmental exposures may be reduced. CONCLUSIONS: Results across EMA studies support the importance of the prenatal and neonatal periods in ASD etiology, and provide evidence for the role of the maternal immune response during pregnancy. Future directions for EMA, and the field of ASD in general, include interrogation of mechanistic pathways and examination of combined effects of exposures. En ligne : http://dx.doi.org/10.1186/s13229-021-00429-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459