Presentation is loading. Please wait.

Presentation is loading. Please wait.

Epigenetic regulation in murine offspring as a novel mechanism for transmaternal asthma protection induced by microbes  Stephanie Brand, PhD, René Teich,

Published byMathilda Bosmans Modified over 4 years ago

Similar presentations

Presentation on theme: "Epigenetic regulation in murine offspring as a novel mechanism for transmaternal asthma protection induced by microbes  Stephanie Brand, PhD, René Teich,"— Presentation transcript:

1 Epigenetic regulation in murine offspring as a novel mechanism for transmaternal asthma protection induced by microbes  Stephanie Brand, PhD, René Teich, PhD, Tanja Dicke, PhD, Hani Harb, BSc, Ali Ö. Yildirim, MD, Jörg Tost, PhD, Regine Schneider- Stock, PhD, Robert A. Waterland, PhD, Uta-Maria Bauer, PhD, Erika von Mutius, MD, MSc, Holger Garn, PhD, Petra I. Pfefferle, PhD, DrPH, Harald Renz, MD  Journal of Allergy and Clinical Immunology  Volume 128, Issue 3, Pages e7 (September 2011) DOI: /j.jaci Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 TH1/TH2 cytokine balance after prenatal A lwoffii F78 exposure. A, Concentrations of IFN-γ, IL-4, IL-5, IL-13, and IL-10 in the supernatant of anti-CD3/anti-CD28–stimulated mononuclear spleen cells from offspring from A lwoffii F78– or sham-exposed (PBS) mothers. B, Relative mRNA expression of IFN-γ, IL-4, IL-5, IL-13, and IL-10 in CD4+CD25− splenic T cells. Data represent the results of 2 independent experiments, each with 4 to 8 individually analyzed animals per group. ∗P < .05, ∗∗P < .01. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 Effects of anti−IFN-γ treatment during OVA challenge in offspring of A lwoffii F78−exposed mothers. A, Differential leukocyte numbers in BAL fluids. B, Quantification of inflammation and mucus-producing goblet cells. C, Airway responsiveness to methacholine (MCH) in offspring. D, In vitro TH2 cytokine production by restimulated mononuclear splenocytes. E, OVA-specific serum antibody levels (n = 8 mice per group). ns, Not significant. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig 3 H4 acetylation within the IFNG and IL4 promoters after prenatal A lwoffii F78 exposure. H4ac and H3K27me3 levels within the IFNG, IL4, and IL5 promoters and the CNS1 region were determined by means of ChIP in CD4+CD25− T cells purified from spleens of offspring from A lwoffii F78– or sham-exposed (PBS) mothers. Data represent the results of 2 independent experiments, each with 4 to 8 individually analyzed animals per group. ns, Not significant. ∗∗P < .01. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5 Fig 4 Effects of garcinol treatment during OVA challenge on H4 acetylation at the IFNG promoter of CD4+CD25− splenic T cells and asthma protection by prenatal A lwoffii F78 exposure. A, H4ac within the IFNG and IL4 promoters and CNS1 (for control groups, see Fig E4). B, Differential leukocyte numbers in BAL fluid. C, Quantification of airway inflammation and mucus-producing goblet cells. D, Airway responsiveness to aerosolized methacholine (MCH). E, In vitro cytokine production by restimulated splenocytes. Gar, Garcinol. Data represent the results of 2 independent experiments, each with 4 to 8 individually analyzed animals per group. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6 Fig E1 H4 acetylation within the STAT-4 promoter after prenatal A lwoffii F78 exposure. H4ac and H3K27me3 levels within the STAT-4 promoter were determined by means of ChIP in CD4+ CD25+ T cells purified from spleens of offspring from A lwoffii F78- or sham-exposed (PBS) mothers. Data represent the results of 2 independent experiments, each with 4 to 8 individually analyzed animals per group. ns, Not significant. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

7 Fig E2 Modulation of DNA methylation within CNS1 in splenic CD4+CD25− T cells from offspring after prenatal A lwoffii F78 exposure. Positions of CpG sites correspond to their positions upstream of the transcription start site of annotated sequence NM_ for IFNG (A), NM_ (IL5), and NM_ (IL4) for IL4 and CNS1 (B). Data represent results of 2 independent experiments, each with 4 to 8 individually analyzed animals per group. ∗P < .05, ∗∗P < .01. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

8 Fig E3 T-cell activation and proliferation after garcinol treatment. A, Ex vivo proliferation of splenic T cells of garcinol- and PBS-treated mice determined by means of CD4+ and CFSE labeling and subsequent FACS analysis. B, In vivo proliferation of splenic CFSE-labeled CD4+ T cells transferred from garcinol- or PBS-treated mice intravenously into BALB/cscid mice determined at day 8 by means of FACS analysis. Data are from 1 representative mouse per group. Two independent experiments were performed, each with 2 to 4 individually analyzed animals per group. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

9 Fig E4 Modulation of H4 acetylation at the IFNG promoter by using the histone acetyltransferase inhibitor garcinol (control groups). H4ac levels within the IFNG and IL4 promoter and CNS1 in CD4+CD25− splenic T cells from offspring treated with garcinol before each OVA challenge were analyzed by means of ChIP. Data represent the results of 2 independent experiments, each with 4 to 8 individually analyzed animals per group. ns, Not significant. Respective data of experimental groups are provided in Fig 4. ns, Not significant. ∗∗P < .01. Journal of Allergy and Clinical Immunology  , e7DOI: ( /j.jaci ) Copyright © 2011 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Download ppt "Epigenetic regulation in murine offspring as a novel mechanism for transmaternal asthma protection induced by microbes  Stephanie Brand, PhD, René Teich,"

Similar presentations

Dual effects of vitamin D–induced alteration of TH1/TH2 cytokine expression  Victor Matheu, MD, Ove Bäck, MD, PhD, Emma Mondoc, BSc, Shohreh Issazadeh-Navikas,

Dual effects of vitamin D–induced alteration of TH1/TH2 cytokine expression  Victor Matheu, MD, Ove Bäck, MD, PhD, Emma Mondoc, BSc, Shohreh Issazadeh-Navikas,
Poly (ADP-ribose) polymerase 14 and its enzyme activity regulates TH2 differentiation and allergic airway disease  Purvi Mehrotra, PhD, Andrew Hollenbeck,

Poly (ADP-ribose) polymerase 14 and its enzyme activity regulates TH2 differentiation and allergic airway disease  Purvi Mehrotra, PhD, Andrew Hollenbeck,
Immunomodulatory effects of aqueous birch pollen extracts and phytoprostanes on primary immune responses in vivo  Jan Gutermuth, MD, Mayte Bewersdorff,

Immunomodulatory effects of aqueous birch pollen extracts and phytoprostanes on primary immune responses in vivo  Jan Gutermuth, MD, Mayte Bewersdorff,
Maternal phthalate exposure promotes allergic airway inflammation over 2 generations through epigenetic modifications  Susanne Jahreis, PhD, Saskia Trump,

Maternal phthalate exposure promotes allergic airway inflammation over 2 generations through epigenetic modifications  Susanne Jahreis, PhD, Saskia Trump,
Maternal immune response to helminth infection during pregnancy determines offspring susceptibility to allergic airway inflammation  Kathrin Straubinger,

Maternal immune response to helminth infection during pregnancy determines offspring susceptibility to allergic airway inflammation  Kathrin Straubinger,
Effective prevention and therapy of experimental allergic asthma using a GATA-3– specific DNAzyme  Serdar Sel, MD, Michael Wegmann, PhD, Tanja Dicke, MSc,

Effective prevention and therapy of experimental allergic asthma using a GATA-3– specific DNAzyme  Serdar Sel, MD, Michael Wegmann, PhD, Tanja Dicke, MSc,
The activating protein 1 transcription factor basic leucine zipper transcription factor, ATF- like (BATF), regulates lymphocyte- and mast cell–driven immune.

The activating protein 1 transcription factor basic leucine zipper transcription factor, ATF- like (BATF), regulates lymphocyte- and mast cell–driven immune.
Let-7 microRNA–mediated regulation of IL-13 and allergic airway inflammation  Manish Kumar, MSc, Tanveer Ahmad, MSc, Amit Sharma, PhD, Ulaganathan Mabalirajan,

Let-7 microRNA–mediated regulation of IL-13 and allergic airway inflammation  Manish Kumar, MSc, Tanveer Ahmad, MSc, Amit Sharma, PhD, Ulaganathan Mabalirajan,
Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model  Sylvie Amu, PhD, Sean P.

Regulatory B cells prevent and reverse allergic airway inflammation via FoxP3-positive T regulatory cells in a murine model  Sylvie Amu, PhD, Sean P.
The activating protein 1 transcription factor basic leucine zipper transcription factor, ATF- like (BATF), regulates lymphocyte- and mast cell–driven immune.

The activating protein 1 transcription factor basic leucine zipper transcription factor, ATF- like (BATF), regulates lymphocyte- and mast cell–driven immune.
Prior airway exposure to allergen increases virus-induced airway hyperresponsiveness  Mika J Mäkelä, MD, Ralph Tripp, PhD, Azzeddine Dakhama, PhD, Jun-Won.

Prior airway exposure to allergen increases virus-induced airway hyperresponsiveness  Mika J Mäkelä, MD, Ralph Tripp, PhD, Azzeddine Dakhama, PhD, Jun-Won.
Maternal allergy increases susceptibility to offspring allergy in association with TH2- biased epigenetic alterations in a mouse model of peanut allergy 

Maternal allergy increases susceptibility to offspring allergy in association with TH2- biased epigenetic alterations in a mouse model of peanut allergy 
Allergy prevention starts before conception: Maternofetal transfer of tolerance protects against the development of asthma  Tobias Polte, PhD, Christian.

Allergy prevention starts before conception: Maternofetal transfer of tolerance protects against the development of asthma  Tobias Polte, PhD, Christian.
Allergic sensitization can be induced via multiple physiologic routes in an adjuvant- dependent manner  David Dunkin, MD, M. Cecilia Berin, PhD, Lloyd.

Allergic sensitization can be induced via multiple physiologic routes in an adjuvant- dependent manner  David Dunkin, MD, M. Cecilia Berin, PhD, Lloyd.
Interferon response factor 3 is essential for house dust mite–induced airway allergy  Thomas Marichal, DVM, Denis Bedoret, DVM, PhD, Claire Mesnil, DVM,

Interferon response factor 3 is essential for house dust mite–induced airway allergy  Thomas Marichal, DVM, Denis Bedoret, DVM, PhD, Claire Mesnil, DVM,
Selective control of SIRP-α–positive airway dendritic cell trafficking through CD47 is critical for the development of TH2-mediated allergic inflammation 

Selective control of SIRP-α–positive airway dendritic cell trafficking through CD47 is critical for the development of TH2-mediated allergic inflammation 
Ting-ting Zhang, MSc, Klaus Okkenhaug, PhD, Baher F

Ting-ting Zhang, MSc, Klaus Okkenhaug, PhD, Baher F
Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity  Jillian L. Barlow, PhD, Agustin Bellosi,

Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity  Jillian L. Barlow, PhD, Agustin Bellosi,
Expression of IL-4 receptor α on smooth muscle cells is not necessary for development of experimental allergic asthma  Frank Kirstein, PhD, William G.C.

Expression of IL-4 receptor α on smooth muscle cells is not necessary for development of experimental allergic asthma  Frank Kirstein, PhD, William G.C.
Frank Kirstein, PhD, Natalie E

Frank Kirstein, PhD, Natalie E

Similar presentations

Ads by Google