Psoriasis is a chronic inflammatory disease affecting 1–3 % of the general population. Traditional systemic therapies for psoriasis, such as methotrexate, have a potential for long-term toxicity and may not always provide sufficient improvement of the condition.
In a recent study by van der Fits et al. a mouse model of dermatitis closely resembling human psoriasis was obtained by the topical application of Imiquimod (IMQ) to mouse ear skin. IMQ, linked to the IL-23/IL-17 axis, can function as a toll-like receptor 7/8 (TLR7/8) ligand and initiate a potent innate immune system response. Mouse skin lesions showed increased epidermal proliferation, abnormal differentiation of keratinocytes, epidermal accumulation of neutrophils in micro-abcesses, neo-angiogenesis, and infiltrates consisting of CD4(+) T cells, CD11c(+) dendritic cells, and plasmacytoid dendritic cells.
In the mouse dermatitis study presented here, in vivo phagocyte-mediated myeloperoxydase (MPO) activity was monitored non-invasively by detecting bioluminescent signal resulting from MPO-specific luminol catabolism. MPOluminol bioluminescence signal is known to be co-localized with histological sites of inflammation as well as infiltration of neutrophils and activated eosinophils.
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