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Human Airway Trypsin-Like Protease Induces PAR-2-Mediated IL-8 Release in Psoriasis Vulgaris
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Human Airway Trypsin-Like Protease Induces PAR-2-Mediated IL-8 Release in Psoriasis Vulgaris
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Journal Article
Human Airway Trypsin-Like Protease Induces PAR-2-Mediated IL-8 Release in Psoriasis Vulgaris
2004
Overview
Human airway trypsin-like protease (HAT), a novel serine protease in the airways, enhances cell growth and IL-8 production. The expression and role of HAT in the skin however, is unknown. Immunofluorescence staining and reverse transcription (RT)-PCR were done to know HAT production in normal and psoriatic tissues and keratinocyte cell lines. Cell growth and/or IL-8 release analyses were made by bromo-deoxyuridine (BrdU) uptake and ELISA. Psoriatic epidermis showed more extensive immunofluorescence expression of HAT, and less extensive expression of protease-activated receptor (PAR)-2. RT-PCR demonstrated a higher HAT and a lesser PAR-2 mRNA expressions in psoriatic epidermis. Normal keratinocyte and epidermoid carcinoma cell lines expressed HAT and PAR-2 mRNA, and immortalized keratinocytes (HaCaT) expressed PAR-2, but not HAT mRNA. PAR-2 was detected along the keratinocyte surface in culture and became invisible upon HAT stimulation, suggesting a process of its internalization. HAT or PAR-2 activating peptide did not enhance BrdU uptake, but induced an IL-8 release. Treatment with HAT and IL-1β synergistically increased the effect of IL-8 release. Inhibition of PAR-2 resulted in a decreased HAT-induced IL-8 release. Thus, HAT might promote PAR-2-mediated IL-8 production to accumulate inflammatory cells in the epidermal layer of psoriasis.
Publisher
Elsevier Inc,Nature Publishing,Elsevier Limited
Subject
/ Aged
/ Biological and medical sciences
/ Biological Transport - drug effects
/ Biopsy
/ Cell Division - drug effects
/ Female
/ human airway trypsin-like protease
/ Humans
/ IL-8
/ Male
/ protease-activated receptor-2
/ Psoriasis. Parapsoriasis. Lichen
/ Receptor, PAR-2 - metabolism
/ Recombinant Proteins - pharmacology
/ Serine Endopeptidases - genetics
/ Serine Endopeptidases - metabolism
