Beneficial antipruritic effects of lowering Interleukin -17 and/or IgE by anti-IgE monoclonal antibodies and PPAR gamma agonist in experimentally induced atopic dermatitis in mice

Document Type : Original Article

Authors

1 Department of Dermatology, Venerology and Andrology; Faculty of Medicine, University of Alexandria, Egypt

2 Department of Dermatology, Venereology and Andrology, Faculty of Medicine, Alexandria University, Egypt

3 Egyptian Ministry of Health Hospitals

4 Department of Medical Physiology, Faculty of Medicine, Alexandria University, Egypt

Abstract

Introduction: Itch is a major complaint in chronic allergic dermatitis. High levels of interleukin -17 (IL -17) and immunoglobulin E (Ig E) have been suspected to play a major role in this inflammatory condition. The aim of this work was to study the potential antipruritic effect of lowering IL-17 and /or IgE by anti IgE monoclonal antibodies and peroxisome proliferator-activated receptor gamma (PPAR γ) agonist in an experimental model of atopic dermatitis (AD) induced by oxazolone in mice. Methods: Fifty female mice were randomly assigned to 4 groups. AD-like lesions were induced in group 2, 3 and 4 by application of 5 % oxazolone followed by 0.1% oxazolone to the mice skin (chronic AD). Group 2 mice were left untreated while those in group 3 and 4 received anti IgE monoclonal antibodies (omalizumab) and PPAR γ agonist (pioglitazone) respectively. Results: Administration of either anti IgE monoclonal antibodies (omalizumab) and PPAR γ agonist (pioglitazone) significantly reduced scratching behavior in treated mice. This was accompanied by significant decrease of the elevated levels of IL-17 and IgE by both drugs. IL-17 suppression was better with pioglitazone while IgE suppression was more significant with omalizumab. Dermoscopic, histological examination and transepidermal water loss (TEWL) also showed significant improvement. Conclusions: Both anti IgE monoclonal antibodies (omalizumab) and PPAR γ agonist (pioglitazone) offer antipruritic effects in AD by reducing IL-17, Ig E and transepidermal water loss.

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