br Discussion Many studies have been carried out

Discussion Many studies have been carried out to determine the pathogenesis of psoriasis; however, its etiology is not yet clear. Many studies have focused on chronic inflammation in psoriasis. In this study, levels of CRP, fibrinogen, and the ESR, which are markers of inflammation, were found to be significantly higher in the patients with psoriasis than in the control group. This supports the view that psoriasis is an inflammatory skin disease (Table 1). Chemerin has been shown to play a part in the inflammatory process. The accumulation of pDCs in psoriatic skin and chemerin/ChemR23 has been shown to be closely correlated. Pro-chemerin is produced primarily by dermal fibroblasts, but also by mast and endothelial cells. After this precursor of chemerin has been secreted, it is activated by enzymes produced by mast angiotensin receptor blocker and neutrophils found in early psoriatic lesions. Zheng et al reported that chemerin was expressed in every layer of normal and arrested epithelium. Chemerin levels were found to be particularly high at the periphery of psoriatic lesions. However, conflicting findings have been reported for the blood levels of chemerin in patients with psoriasis. A group of researchers has established higher levels of serum chemerin in patients with psoriasis than in healthy controls. In contrast, Xue et al established significantly lower levels of circulating chemerin in patients with psoriasis than in healthy controls. Based on our findings, serum chemerin levels in patients with psoriasis were significantly higher than in the control group (p < 0.01) (Table 1). A different, but supporting, finding was that chemerin levels were significantly higher in the patients with moderate and severe psoriasis than in patients with mild psoriasis (p < 0.05 and p < 0.01, respectively) (Table 2). Chemerin production during skin inflammation may therefore be an important source of circulating chemerin. It has been shown that ChemR23 receptors are upregulated by proinflammatory cytokines such as TNF-α, IL-1β, and IL-6. Recombinant chemerin has also been reported to enhance the production of many proinflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8). Correlation analysis performed in this study established a positive correlation between chemerin levels and the inflammatory markers CRP and the WBC count and the PASI score, which indicates disease activity (Table 3). These findings showed that chemerin was increased in the acute response and was correlated with disease activity in psoriasis. Gisondi et al and Lora et al established a positive correlation between serum chemerin levels in patients with psoriasis and levels of CRP. A positive correlation was also reported between chemerin and proinflammatory cytokines, including IL-6, TNF-α, and leptin and there was a positive correlation between chemerin and the WBC count. Therefore it was suggested that chemerin produced as an inflammatory response might play an active part in regulating the activity of other inflammatory cells and in cytokine production. Nishibu et al established that monocytes were the most prominent cellular resource in psoriasis and there is a close correlation between increased cytokine levels and the severity of skin lesions. Psoriatic tissue lesions occur as a result of keratinocyte proliferation and the over expression of the S100 protein family, which regulates cell signals, to accumulate inflammatory cells. Studies measuring the calprotectin levels in patients with psoriasis are considered to be insufficient. Garcia-Rodriguez et al established high levels of plasma calprotectin; however, this result was not statistically significant. Aochi et al and Benoit et al found significantly higher levels of serum calprotectin in patients with psoriasis compared with a control group. In this study, we found that serum calprotectin levels in patients with psoriasis were significantly higher than in the control group (p < 0.001) (Table 1). Calprotectin levels in the patients with severe psoriasis were significantly higher than those in the patients with mild psoriasis (p < 0.05) (Table 2). In a similar manner, Benoit et al established high levels of calprotectin in patients with psoriasis with high disease activity. Patients with arthritis and inflammation were excluded from our study and the high levels of calprotection were considered to be a remarkable finding.