Silencing Of Mir-155 Suppresses Inflammatory Responses In Psoriasis Through Inflammasome Nlrp3 Regulation

Psoriasis is a dermatosis with the major clinical symptoms of scale, erythema and itching, and it has a long disease course. In addition, it is easily recurrent and refractory, greatly affecting the physical and mental health of patients. In the present study, it was hypothesized that the function of miR-155 increases psoriasis-induced inflammation and that its expression may be dependent on inflammasome activation. miR-155 expression was examined by gene chip array and quantitative polymerase chain reaction analysis. miR-155 expression levels were significantly increased in an in vivo model of psoriasis compared with normal tissues, as was the expression of NLR family pyrin domain containing 3 (NLRP3). In vitro, using keratinocyte-induced HaCaT cells as a model for psoriasis, silencing of miR-155 was confirmed to significantly decrease inflammation and NLRP3/caspase-1 signaling. Activation of toll-like receptor 4 (TLR4) enhanced the miR-155-induced inflammatory response in the in vitro keratinocyte model. Treatment with a TLR4 inhibitor or an NLRP3 inhibitor reversed the miR-155-mediated inflammation in the same cell system. The present study demonstrated that miR-155 silencing suppressed psoriasis-associated inflammatory responses through inflammasome NLRP3 regulation.