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Peroxisome proliferator-activated receptor α regulates skin inflammation and humoral response in atopic dermatitis  Delphine Staumont-Sallé, MD, Georges.

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Presentation on theme: "Peroxisome proliferator-activated receptor α regulates skin inflammation and humoral response in atopic dermatitis  Delphine Staumont-Sallé, MD, Georges."— Presentation transcript:

1 Peroxisome proliferator-activated receptor α regulates skin inflammation and humoral response in atopic dermatitis  Delphine Staumont-Sallé, MD, Georges Abboud, BSc, Céline Brénuchon, MD, Akira Kanda, MD, PhD, Thomas Roumier, PhD, Céline Lavogiez, MD, Sébastien Fleury, Patrick Rémy, Jean-Paul Papin, Justine Bertrand-Michel, François Tercé, PhD, Bart Staels, PhD, Emmanuel Delaporte, MD, Monique Capron, PhD, David Dombrowicz, PhD  Journal of Allergy and Clinical Immunology  Volume 121, Issue 4, Pages e6 (April 2008) DOI: /j.jaci Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 Increased skin inflammation in PPAR-α−/− mice in a model of AD. A, Hematoxylin and eosin staining of skin sections from OVA-sensitized mice or PBS-treated PPAR-α−/− or WT mice (original magnification ×100). B, Epidermal thickness. C, Eosinophil, mast cell, and T-lymphocyte numbers in dermis at the site of sensitization and treatment (n = 6-10 animals per group). Data are expressed as means ± SEMs. ∗Statistically different from PBS-treated mice (P < .05). $, Statistically different from WT mice (P < .05). D, Skin cytokine, chemokine, and receptor expression. E, Skin NF-κB 1 and 2 expression. Primers used are listed in Table E1 in the Online Repository at Results for OVA-sensitized animals are expressed as a fold increase compared with the identically responding PBS-treated animals (n = 3-6 animals per group). $, Statistically different from OVA-sensitized WT mice (P < .05). Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 Increased lung inflammation and humoral response in PPAR-α−/− mice in a model of AD. A, Measurement of AHR to increasing methacholine concentrations by means of whole-body plethysmography. B, Total number of macrophages, neutrophils, lymphocytes, and eosinophils in BAL fluid at the time of death (n = 3-6 animals per group). C, Total IgE, IgG1, and IgG2a serum concentrations. D, OVA-induced cytokine production by inguinal lymph nodes in vitro (n = 6-10 animals per group). ∗Statistically different from PBS-treated mice (P < .05). $, Statistically different from WT mice (P < .05). Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig 3 Decreased expression of PPAR-α in lesional skin from patients with AD. RNA was extracted from skin biopsy specimens of nontreated patients with AD (n = 8) and nonatopic healthy individuals (n = 6). Real-time PCR analysis of PPAR-α and PPAR-β/δ expression was conducted by using the primers shown in Table E1. $, Statistically different from control individuals (P < .05). Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5 Fig 4 Improvement of skin lesions in a model of AD after topical treatment with the PPAR-α agonist WY A, Hematoxylin and eosin staining of skin sections from OVA-sensitized or PBS-treated mice treated with dimethyl sulfoxide (DMSO) or WY14643 (original magnification ×200). B, Epidermal thickness. C, CD4 T-cell, eosinophil, and mast cell numbers in dermis at the site of sensitization and treatment. D. Skin cytokine, chemokine, and receptor expression. Primers used are listed in Table E1. E, Skin NF-κB 1 and 2 expression (n = 6-10 animals per group). ∗Statistically different from PBS-treated mice (P < .05). $, Statistically different from DMSO-treated mice (P < .05). Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6 Analysis of skin barrier function in WT and PPAR-α−/− mice and PPAR-α agonist–treated WT animals in a model of AD. A, Nile red staining of skin neutral lipids (200-fold magnification). B and C, TEWL. D and E, Skin lipid content (n = 4 animals per group). $, Statistically different from dimethyl sulfoxide (DMSO)–treated mice (P < .05). Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

7 Humoral and cellular response in WT and PPAR-α−/− mice and PPAR-α agonist–treated WT animals in a model of AD. A, OVA-specific IgE, IgG1, and IgG2a concentrations in WT and PPAR-α−/− mice. B-D, Cytokine production by splenocytes (Fig E2, B and C) and inguinal lymph nodes (Fig E2, D) from PPAR-α−/− and WT mice (Fig E2, B) and WY or dimethyl sulfoxide (DMSO)–treated WT mice (Fig E2, C and D) after in vitro OVA restimulation (n = 5-6 animals per group). E, OVA-specific IgE and IgG1 concentrations in WY or DMSO-treated mice. OVA-specific IgG2a levels remained undetectable. ∗Statistically different from PBS-treated mice (P < .05). $, Statistically different from control WT mice (P < .05). Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

8 Decreased lung inflammation in a model of AD after topical treatment with the PPAR-α agonist WY The total number of macrophages, neutrophils, lymphocytes, and eosinophils in BAL fluid at the time of death is shown (n = 3-6 animals per group). DMSO, Dimethyl sulfoxide. Journal of Allergy and Clinical Immunology  , e6DOI: ( /j.jaci ) Copyright © 2008 American Academy of Allergy, Asthma & Immunology Terms and Conditions

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