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Co-activation of glucocorticoid receptor and peroxisome proliferator-activated receptor-γ in murine skin prevents worsening of atopic march

Julie Deckers (UGent) , Nadia Bougarne (UGent) , Viacheslav Mylka (UGent) , Sofie Desmet (UGent) , Astrid Luypaert (UGent) , Michael Devos (UGent) , Giel Tanghe (UGent) , Justine Van Moorleghem (UGent) , Manon Vanheerswynghels (UGent) , Lode De Cauwer (UGent) , et al.
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Abstract
Children with atopic dermatitis show an increased risk to develop asthma later in life, a phenomenon referred to as "atopic march," which emphasizes the need for secondary prevention therapies. This study aimed to investigate whether relief of skin inflammation by glucocorticoids and peroxisome proliferator-activated receptor agonists might influence the subsequent development of asthma in a murine model for the atopic march in which mice were repeatedly exposed to house dust mite via the skin, followed by exposure to house dust mite in lungs. To abrogate atopic dermatitis, mice received topical treatment with glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma agonists. Nuclear receptor ligand effects were assessed on primary keratinocytes and dendritic cells, as central players in skin inflammation. Prior house dust mite-induced skin inflammation aggravates allergic airway inflammation and induces a mixed T helper type 2/T helper type 17 response in the lungs. Cutaneous combined activation of glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma reduced skin inflammation to a higher extent compared to single activation. Additive anti-inflammatory effects were more prominent in dendritic cells, as compared to keratinocytes. Alleviation of allergic skin inflammation by activation of glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma appeared insufficient to avoid the allergic immune response in the lungs, but efficiently reduced asthma severity by counteracting the Th17 response. Glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma co-activation represents a potent remedy against allergic skin inflammation and worsening of atopic march.
Keywords
HOUSE-DUST MITE, AGGRAVATES EXPERIMENTAL ASTHMA, MOUSE BONE-MARROW, DENDRITIC CELLS, ALLERGIC SENSITIZATION, PPAR-ALPHA, KAPPA-B, GM-CSF, DERMATITIS, TRANSACTIVATION

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Chicago
Deckers, Julie, Nadia Bougarne, Viacheslav Mylka, Sofie Desmet, Astrid Luypaert, Michael Devos, Giel Tanghe, et al. 2018. “Co-activation of Glucocorticoid Receptor and Peroxisome Proliferator-activated Receptor-γ in Murine Skin Prevents Worsening of Atopic March.” Journal of Investigative Dermatology 138 (6): 1360–1370.
APA
Deckers, J., Bougarne, N., Mylka, V., Desmet, S., Luypaert, A., Devos, M., Tanghe, G., et al. (2018). Co-activation of glucocorticoid receptor and peroxisome proliferator-activated receptor-γ in murine skin prevents worsening of atopic march. JOURNAL OF INVESTIGATIVE DERMATOLOGY, 138(6), 1360–1370.
Vancouver
1.
Deckers J, Bougarne N, Mylka V, Desmet S, Luypaert A, Devos M, et al. Co-activation of glucocorticoid receptor and peroxisome proliferator-activated receptor-γ in murine skin prevents worsening of atopic march. JOURNAL OF INVESTIGATIVE DERMATOLOGY. 2018;138(6):1360–70.
MLA
Deckers, Julie, Nadia Bougarne, Viacheslav Mylka, et al. “Co-activation of Glucocorticoid Receptor and Peroxisome Proliferator-activated Receptor-γ in Murine Skin Prevents Worsening of Atopic March.” JOURNAL OF INVESTIGATIVE DERMATOLOGY 138.6 (2018): 1360–1370. Print.
@article{8548945,
  abstract     = {Children with atopic dermatitis show an increased risk to develop asthma later in life, a phenomenon referred to as {\textacutedbl}atopic march,{\textacutedbl} which emphasizes the need for secondary prevention therapies. This study aimed to investigate whether relief of skin inflammation by glucocorticoids and peroxisome proliferator-activated receptor agonists might influence the subsequent development of asthma in a murine model for the atopic march in which mice were repeatedly exposed to house dust mite via the skin, followed by exposure to house dust mite in lungs. To abrogate atopic dermatitis, mice received topical treatment with glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma agonists. Nuclear receptor ligand effects were assessed on primary keratinocytes and dendritic cells, as central players in skin inflammation. Prior house dust mite-induced skin inflammation aggravates allergic airway inflammation and induces a mixed T helper type 2/T helper type 17 response in the lungs. Cutaneous combined activation of glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma reduced skin inflammation to a higher extent compared to single activation. Additive anti-inflammatory effects were more prominent in dendritic cells, as compared to keratinocytes. Alleviation of allergic skin inflammation by activation of glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma appeared insufficient to avoid the allergic immune response in the lungs, but efficiently reduced asthma severity by counteracting the Th17 response. Glucocorticoid receptor/peroxisome proliferator-activated receptor-gamma co-activation represents a potent remedy against allergic skin inflammation and worsening of atopic march.},
  author       = {Deckers, Julie and Bougarne, Nadia and Mylka, Viacheslav and Desmet, Sofie and Luypaert, Astrid and Devos, Michael and Tanghe, Giel and Van Moorleghem, Justine and Vanheerswynghels, Manon and De Cauwer, Lode and Thommis, Jonathan and Vuylsteke, Marnik and Tavernier, Jan and Lambrecht, Bart and Hammad, Hamida and De Bosscher, Karolien},
  issn         = {0022-202X},
  journal      = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
  language     = {eng},
  number       = {6},
  pages        = {1360--1370},
  title        = {Co-activation of glucocorticoid receptor and peroxisome proliferator-activated receptor-\ensuremath{\gamma} in murine skin prevents worsening of atopic march},
  url          = {http://dx.doi.org/10.1016/j.jid.2017.12.023},
  volume       = {138},
  year         = {2018},
}

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