RABEONY H., POHIN M., VASSEUR P., PETIT-PARIS I., JÉGOU JF., FAVOT L., FROUIN E., BOUTET MA., BLANCHARD F., TOGBE D., RYFFEL B., BERNARD FX., LECRON JC., MOREL F. (2015)
IMQ-induced skin inflammation in mice is dependent on IL-1R1 and MyD88 signaling but independent of the NLRP3 inflammasome.
European Journal of Immunology, Volume 45, Issue 7

OBJECTIVE

The pathogenesis of inflammatory skin diseases such as psoriasis involves the release of numerous proinflammatory cytokines, including members of the IL-1 family. Here we report overexpression of IL-1α, IL-1β, and IL-1 receptor antagonist (IL-1Ra) mRNA, associated to expression of IL-23p19, IL-17A and IL-22 in skin cells, upon topical application of the TLR7 agonist imiquimod (IMQ) in C57BL/6J mice.

METHODS:

Mice were bred in the animal facility of Centre National de la Recherche Scientifique (TAMM, Institute Transgenose, Orléans, France) and were kept under specific pathogen-free conditions and provided food and water ad libitum. Experimental procedures were approved by French Government’s ethical and animal experiment regulations. Mice at 8-10 weeks of age were used in those experiments. Back skin of the mice was shaved and remaining hairs were removed using a depilatory cream (Veet@, Reckitt Benckiser, France). Psoriasis-like skin disease was induced as described previously by van der Fits et al [17]. Shaved back skin and right ear were daily treated with 62.5 mg Aldara@ cream (5% imiquimod, 3M pharmaceuticals) for 6 days. Control mice were treated similarly with vaseline (VAS) (Vaseline Lanette cream, Fagron). Due to deshydratation and weight loss observed in IMQ-treated mice, a daily volume substitution by intraperitoneal injection of 300 μl sterile PBS was performed from day 1 to 5 in all experimental groups.

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