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IL-36 cytokine expression and its relationship with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions

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Summary

This study examined the correlation of the expression of interleukin-36 (IL-36), a novel member of interleukin-1 (IL-1) family, with p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor-kappa B (NF-κB) pathways in psoriasis vulgaris skin lesions. The expression levels of IL-36α, IL-36β, IL-36Γ, phosphorylated p38 MAPK, and NF-κBp65 were detected in the skin tissues of 38 psoriasis patients and 17 healthy control subjects by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting. The cytokine expression levels were compared between the psoriasis group and the control group. A correlation analysis between cytokine proteins was performed in the psoriasis group. Results showed that the expression levels of IL-36a, IL-36β, IL-36Γ, phosphorylated p38 MAPK and NF-κBp65 in the psoriasis group were significantly higher than those in the control group (P<0.001). In the psoriasis group, the IL-36 cytokine expression was positively correlated with phosphorylated p38 MAPK and NF-κBp65 expression (P<0.05). A significant positive correlation was also found between the phosphorylated p38 MAPK and NF-κBp65 expression (P<0.01). It was concluded that the increased IL-36 expression is correlated with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions. All the three factors may be jointly involved in the pathogenesis and local inflammatory response of psoriasis.

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Correspondence to Jia-wen Li  (李家文).

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Both authors contributed equally to this work.

This project was supported by grants from the National Natural Science Foundation of China (No. 30972654, No. 81101191, No. 81271765 and No. 81171495).

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He, Q., Chen, Hx., Li, W. et al. IL-36 cytokine expression and its relationship with p38 MAPK and NF-κB pathways in psoriasis vulgaris skin lesions. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 33, 594–599 (2013). https://doi.org/10.1007/s11596-013-1164-1

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  • DOI: https://doi.org/10.1007/s11596-013-1164-1

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