AI Article Synopsis
- This study investigated the roles of TRPA1 and TRPV1 channels in a mouse model of psoriasis induced by imiquimod, using selective antagonists and genetically modified mice.
- Findings showed that TRPA1 knockout mice displayed worsened psoriasis symptoms, while inhibiting TRPV1 led to symptom reduction, highlighting TRPV1's primary role in the process.
- The research indicated that activation of TRPA1 could potentially have protective effects in psoriasiform dermatitis, suggesting its significance alongside TRPV1 in mediating skin responses.
Article Abstract
This study revealed the modulatory role of transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) cation channels in the Aldara-induced (5% imiquimod) murine psoriasis model using selective antagonists and genetically altered animals. We have also developed a refined localized model to enable internal controls and reduce systemic effects. Skin pathology was quantified by measuring skin thickness, scaling, blood flow, and analyzing dermal cellular infiltrate, whereas nocifensive behaviors were also observed. Cytokine gene expression profiles were measured ex vivo. Psoriasiform dermatitis was significantly enhanced in TRPA1 knockout mice and with TRPA1 antagonist (A967079) treatment. By comparison, symptoms were decreased when TRPV1 function was inhibited. Imiquimod induced Ca influx in TRPA1-, but not in TRPV1-expressing cell lines. Immunohistochemical studies revealed that CD4+ T helper cells express TRPA1 but not TRPV1 ion channels in mice skin. Compared with the TRPV1 knockout animals, additional elimination of the TRPA1 channels in the TRPV1/TRPA1 double knockout mice did not modify the outcome of the imiquimod-induced reaction, further supporting the dominant role of TRPV1 in the process. Our results suggest that the protective effects in psoriasiform dermatitis can be mediated by the activation of neuronal and nonneuronal TRPA1 receptors.
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| http://dx.doi.org/10.1016/j.jid.2018.02.040 | DOI Listing |
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