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  1. Article ; Online: Postnatal administration of S-adenosylmethionine restores developmental AHR activation-induced deficits in CD8+ T cell function during influenza A virus infection.

    Post, Christina M / Myers, Jason R / Winans, Bethany / Lawrence, B Paige

    Toxicological sciences : an official journal of the Society of Toxicology

    2023  

    Abstract: Developmental exposures can influence life-long health; yet, counteracting negative consequences is challenging due to poor understanding of cellular mechanisms. The aryl hydrocarbon receptor (AHR) binds many small molecules, including numerous ... ...

    Abstract Developmental exposures can influence life-long health; yet, counteracting negative consequences is challenging due to poor understanding of cellular mechanisms. The aryl hydrocarbon receptor (AHR) binds many small molecules, including numerous pollutants. Developmental exposure to the signature environmental AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) significantly dampens adaptive immune responses to influenza A virus (IAV) in adult offspring. CD8+ cytotoxic T lymphocytes (CTL) are crucial for successful infection resolution, which depends on the number generated and the complexity of their functionality. Prior studies showed developmental AHR activation significantly reduced the number of virus-specific CD8+ T cells, but impact on their functions is less clear. Other studies showed developmental exposure was associated with differences in DNA methylation in CD8+ T cells. Yet, empirical evidence that differences in DNA methylation are causally related to altered CD8+ T cell function is lacking. The two objectives were to ascertain whether developmental AHR activation affects CTL function, and whether differences in methylation contribute to reduced CD8+ T cell responses to infection. Developmental AHR triggering significantly reduced CTL polyfunctionality, and modified the transcriptional program of CD8+ T cells. S-adenosylmethionine (SAM), which increases DNA methylation, but not Zebularine, which diminishes DNA methylation, restored polyfunctionality and boosted the number of virus-specific CD8+ T cells. These findings suggest that diminished methylation, initiated by developmental exposure to an AHR-binding chemical, contributes to durable changes in antiviral CD8+ CTL functions later in life. Thus, deleterious consequence of development exposure to environmental chemicals are not permanently fixed, opening the door for interventional strategies to improve health.
    Language English
    Publishing date 2023-02-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfad019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: DNA Methylation Patterns in

    Burke, Catherine G / Myers, Jason R / Post, Christina M / Boulé, Lisbeth A / Lawrence, B Paige

    Environmental health perspectives

    2021  Volume 129, Issue 1, Page(s) 17007

    Abstract: Background: Early life environmental exposures can have lasting effects on the function of the immune system and contribute to disease later in life. Epidemiological studies have linked early life exposure to xenobiotics that bind the aryl hydrocarbon ... ...

    Abstract Background: Early life environmental exposures can have lasting effects on the function of the immune system and contribute to disease later in life. Epidemiological studies have linked early life exposure to xenobiotics that bind the aryl hydrocarbon receptor (AhR) with dysregulated immune responses later in life. Among the immune cells influenced by developmental activation of the AhR are
    Objective: Our goal was to identify cellular mechanisms that drive impaired
    Methods: C57BL/6 mice were vertically exposed to the prototype AhR ligand, 2,3,7,8-tetrachlorodibenzo-
    Results: Gene and protein expression showed that developmental AhR activation reduced
    Discussion: Taken together, these results indicate that skewed DNA methylation is one of the mechanisms by which early life exposures can durably change the function of T cells in mice. Furthermore, treatment with DNA methylation-altering drugs after the exposure restored some aspects of
    MeSH term(s) Animals ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; DNA Methylation/drug effects ; Environmental Exposure ; Female ; Influenza A virus/immunology ; Mice ; Mice, Inbred C57BL ; Orthomyxoviridae Infections/immunology ; Polychlorinated Dibenzodioxins/toxicity ; Pregnancy ; Receptors, Aryl Hydrocarbon/immunology ; Receptors, Aryl Hydrocarbon/metabolism
    Chemical Substances Polychlorinated Dibenzodioxins ; Receptors, Aryl Hydrocarbon
    Language English
    Publishing date 2021-01-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/EHP7699
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Dung biomass smoke exposure impairs resolution of inflammatory responses to influenza infection.

    McCarthy, Claire E / Duffney, Parker F / Nogales, Aitor / Post, Christina M / Lawrence, B Paige / Martinez-Sobrido, Luis / Thatcher, Thomas H / Phipps, Richard P / Sime, Patricia J

    Toxicology and applied pharmacology

    2022  Volume 450, Page(s) 116160

    Abstract: Epidemiological studies associate biomass smoke with an increased risk for respiratory infections in children and adults in the developing world, with 500,000 premature deaths each year attributed to biomass smoke-related acute respiratory infections ... ...

    Abstract Epidemiological studies associate biomass smoke with an increased risk for respiratory infections in children and adults in the developing world, with 500,000 premature deaths each year attributed to biomass smoke-related acute respiratory infections including infections caused by respiratory viruses. Animal dung is a biomass fuel of particular concern because it generates more toxic compounds per amount burned than wood, and is a fuel of last resort for the poorest households. Currently, there is little biological evidence on the effects of dung biomass smoke exposure on immune responses to respiratory viral infections. Here, we investigated the impact of dung biomass exposure on respiratory infection using a mouse model of dung biomass smoke and cultured primary human small airway epithelial cells (SAECs). Mice infected with influenza A virus (IAV) after dung biomass smoke exposure had increased mortality, lung inflammation and virus mRNA levels, and suppressed expression of innate anti-viral mediators compared to air exposed mice. Importantly, there was still significant tissue inflammation 14 days after infection in dung biomass smoke-exposed mice even after inflammation had resolved in air-exposed mice. Dung biomass smoke exposure also suppressed the production of anti-viral cytokines and interferons in cultured SAECs treated with poly(I:C) or IAV. This study shows that dung biomass smoke exposure impairs the immune response to respiratory viruses and contributes to biomass smoke-related susceptibility to respiratory viral infections, likely due to a failure to resolve the inflammatory effects of biomass smoke exposure.
    MeSH term(s) Animals ; Biomass ; Child ; Humans ; Inflammation/chemically induced ; Inflammation/metabolism ; Influenza, Human ; Pneumonia ; Respiratory Tract Infections
    Language English
    Publishing date 2022-07-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2022.116160
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The Ancestral Environment Shapes Antiviral CD8

    Post, Christina M / Boule, Lisbeth A / Burke, Catherine G / O'Dell, Colleen T / Winans, Bethany / Lawrence, B Paige

    iScience

    2019  Volume 20, Page(s) 168–183

    Abstract: Recent studies have linked health fates of children to environmental exposures of their great grandparents. However, few studies have considered whether ancestral exposures influence immune function across generations. Here, we report transgenerational ... ...

    Abstract Recent studies have linked health fates of children to environmental exposures of their great grandparents. However, few studies have considered whether ancestral exposures influence immune function across generations. Here, we report transgenerational inheritance of altered T cell responses resulting from maternal (F0) exposure to the aryl hydrocarbon receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Since F0 exposure to TCDD has been linked to transgenerational transmission of reproductive problems, we asked whether maternal TCDD exposure also caused transgenerational changes in immune function. F0 exposure caused transgenerational effects on the CD8
    Language English
    Publishing date 2019-09-14
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2019.09.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Early life exposures shape the CD4

    Burke, Catherine G / Myers, Jason R / Boule, Lisbeth A / Post, Christina M / Brookes, Paul S / Lawrence, B Paige

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 11489

    Abstract: Early life environmental exposures drive lasting changes to the function of the immune system and can contribute to disease later in life. One of the ways environmental factors act is through cellular receptors. The aryl hydrocarbon receptor (AHR) is ... ...

    Abstract Early life environmental exposures drive lasting changes to the function of the immune system and can contribute to disease later in life. One of the ways environmental factors act is through cellular receptors. The aryl hydrocarbon receptor (AHR) is expressed by immune cells and binds numerous xenobiotics. Early life exposure to chemicals that bind the AHR impairs CD4
    MeSH term(s) Adult ; Animals ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Cell Differentiation/immunology ; Cell Proliferation ; Child ; Child Development ; Disease Models, Animal ; Environmental Pollutants/immunology ; Female ; Humans ; Influenza A virus/immunology ; Influenza, Human/blood ; Influenza, Human/immunology ; Influenza, Human/virology ; Ligands ; Male ; Mice ; Mitochondrial Dynamics/immunology ; RNA-Seq ; Receptors, Aryl Hydrocarbon/metabolism ; Transcriptome/immunology
    Chemical Substances Ahr protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Environmental Pollutants ; Ligands ; Receptors, Aryl Hydrocarbon
    Language English
    Publishing date 2019-08-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-47866-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Linking the aryl hydrocarbon receptor with altered DNA methylation patterns and developmentally induced aberrant antiviral CD8+ T cell responses.

    Winans, Bethany / Nagari, Anusha / Chae, Minho / Post, Christina M / Ko, Chia-I / Puga, Alvaro / Kraus, W Lee / Lawrence, B Paige

    Journal of immunology (Baltimore, Md. : 1950)

    2015  Volume 194, Issue 9, Page(s) 4446–4457

    Abstract: Successfully fighting infection requires a properly tuned immune system. Recent epidemiological studies link exposure to pollutants that bind the aryl hydrocarbon receptor (AHR) during development with poorer immune responses later in life. Yet, how ... ...

    Abstract Successfully fighting infection requires a properly tuned immune system. Recent epidemiological studies link exposure to pollutants that bind the aryl hydrocarbon receptor (AHR) during development with poorer immune responses later in life. Yet, how developmental triggering of AHR durably alters immune cell function remains unknown. Using a mouse model, we show that developmental activation of AHR leads to long-lasting reduction in the response of CD8(+) T cells during influenza virus infection, cells critical for resolving primary infection. Combining genome-wide approaches, we demonstrate that developmental activation alters DNA methylation and gene expression patterns in isolated CD8(+) T cells prior to and during infection. Altered transcriptional profiles in CD8(+) T cells from developmentally exposed mice reflect changes in pathways involved in proliferation and immunoregulation, with an overall pattern that bears hallmarks of T cell exhaustion. Developmental exposure also changed DNA methylation across the genome, but differences were most pronounced following infection, where we observed inverse correlation between promoter methylation and gene expression. This points to altered regulation of DNA methylation as one mechanism by which AHR causes durable changes in T cell function. Discovering that distinct gene sets and pathways were differentially changed in developmentally exposed mice prior to and after infection further reveals that the process of CD8(+) T cell activation is rendered fundamentally different by early life AHR signaling. These findings reveal a novel role for AHR in the developing immune system: regulating DNA methylation and gene expression as T cells respond to infection later in life.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; DNA Methylation ; Disease Models, Animal ; Female ; Gene Expression Profiling ; Male ; Mice ; Mice, Knockout ; Promoter Regions, Genetic ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/metabolism ; Virus Diseases/genetics ; Virus Diseases/immunology ; Virus Diseases/metabolism
    Chemical Substances Receptors, Aryl Hydrocarbon
    Language English
    Publishing date 2015-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1402044
    Database MEDical Literature Analysis and Retrieval System OnLINE

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