| Psoriasis is a chronic skin disease characterized by abnormal keratinocyte proliferation and prominent inflammatory. Though the precise pathogenesis is not yet understood, a large body of evidence indicates that the immune system plays an important role in the pathogenesis of psoriasis, and the expression of cytokines in psoriatic lesion is imbalance. Along with the establishment of modern concept of immuno-inflammatory system in psoriasis, keratinocytes are well known as biologically active cells, not only for keratin synthesis, but also for immunological functions. Diverse environmental stimuli including UV,LPS and productions of bacteria or virus, trigger a cutaneous inflammatory response by directly inducing KCs to elaborate special pro-inflammatory cytokines and adhesion molecules. There is increasing evidence that special immunologically active products of KCs generated in response to environmental stimuli may orchestrate the initiation of cutaneous inflammation. KC is the concentrator of pathology and clinical behave in psoriasis, and plays a major role in the pathogenesis of psoriasis.HN2 and UV are effective in the treatment of psoriasis, but little is known about their mechanism of action. The aim of our study is to observe the effect of HN2 and UV on cytokines secretion of human keratinocyte HaCaT cell line, both normal and stimulated by PMA/LPS, in order to investigate the mechanism of action, offer theoretics for clinic.In the first part, we built the inflammatory model of HaCaT cell line in vitro using PMA/LPS as stimulators, in order to study the effect of HN2 on cytokines secretion of HaCaT cell line, both normal and stimulated. The results indicated that HaCaT cell secreted IL-1α,IL-2,IL-6 and IL-8 spontaneously; Stimulation by PMA /LPS induced significant increase in IL-6 and IL-8 level and decrease in IL-1α levelin HaCaT cell, a pattern similar to those seen in psoriasis. On HaCaT cell, HN2 increased the secretion of IL-1α,IL-6 and IL-8 distinctly, they may participate in the inflammation of HN2 on normal skin. On HaCaT cell stimulated with PMA/LPS, HN2 decreased the secretion of IL-6,IL-8 and increased the secretion of IL-1α in a low concentration, these suggested that the mechanism of HN2 therapy on psoriasis is related to IL-1α,IL-6 and IL-8, but the secretion of IL-6,IL-8 and IL-1α in stimulated HaCaT cell were significantly increased when HN2 was in a high concentration. These results suggested that the concentration of HN2 for treatment shouldn't be higher, otherwise it would induce inflammation in normal skin as well as in inflammatory skin. In the second part, we studied the effect of UV on cytokines secretion of HaCaT cell line, both normal and stimulated. The results indicated that UV had no influence on the secretion of IL-1α,IL-2 and IL-6 in HaCaT cell, but it could enhance the secretion of IL-8. These suggested that IL-8 takes part in the formation of erythma when normal skin was under the irradiation of UV. UV increased the secretion of IL-1α,IL-6 and IL-8 in HaCaT cell stimulated by PMA/LPS markedly, suggested that the action of UV on psoriasis wasn't by the way of inhabited the secretion of IL-1α,IL-6 and IL-8. Our results suggested that mechanisms of HN2 and UV on psoriasis are different.We merely focus our attention on studying the effect of HN2 and UV on the secretion of IL-1α,IL-2,sIL-2R,IL-6 and IL-8 of KC, it's only one part of cytokine network of immumo-inflammatory pathogenesis in psoriasis. Although KCs play a major role in the pathogenesis of psoriasis, the status of lymphocyte and LC mustn't be neglected. Further study is needed to investigate the precise pathogenesis of psoriasis and the mechanism of action of HN2 and UV on psoriasis. |
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