Erlotinib-Induced Skin Inflammation Is IL-1 Mediated in KC-Tie2 Mice and Human Skin Organ Culture

    October 2014 in “ ˜The œjournal of investigative dermatology/Journal of investigative dermatology ”
    Nicole L. Ward, Narasimharao Bhagathavula, Andrew Johnston, Sean M. Dawes, Wen Fu, Sylviane Lambert, Michael K. Dame, Roscoe L. Warner, Jóhann E. Guðjónsson, James Varani, James T. Elder
    Studysummary This study suggests that erlotinib exacerbates inflammation in a mouse model of skin disease and that IL-1 inhibition could mitigate skin-related side effects of EGFR inhibitors. Our plain-language summary of this paper — not a Tressless recommendation.
    The study investigated the mechanism behind erlotinib-induced skin inflammation using KC-Tie2 mice and human skin organ culture. It concluded that the inflammation was mediated by interleukin-1 (IL-1). Erlotinib treatment increased epidermal thickness and immune cell infiltration in KC-Tie2 mice, which was mitigated by the IL-1 receptor antagonist anakinra. Similarly, in human skin cultures, erlotinib-induced epidermal thickening and pro-inflammatory markers were blocked by anakinra. These findings suggested that IL-1 mediated the inflammatory effects of erlotinib, highlighting the potential of IL-1 inhibition to alleviate skin toxicity in patients undergoing EGFR inhibitor therapy.
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