title: Arazyme inhibits cytokine expression and upregulates skin barrier protein expression.
abstract: In the present study, the inhibitory effect of arazyme on allergic inflammation was investigated by evaluating the alteration of cytokine production and expression of skin barrier proteins in immune and HaCaT human keratinocyte cells. THP‑1 human monocytic and EoL‑1 human eosinophilic cells were treated with Dermatophagoides pteronissinus extract (DpE). Monocyte chemotactic protein‑1 (MCP‑1)/CCL2, interleukin (IL)‑6 and IL‑8 increased following DpE treatment and arazyme significantly blocked the increase of MCP‑1, IL‑6 and IL‑8 expression in cell types. Secretion of MCP‑1, IL‑6 and IL‑8 induced by lipopolysaccharide in THP‑1 cells was also inhibited by arazyme treatment. Arazyme inhibited the secretion of IL‑6 and IL‑8 due to phorbol 12‑myristate 13‑acetate and calcium ionophores in human mast cells. Arazyme blocked the secretion of thymus and activation‑regulated chemokine (TARC)/CCL17, MCP‑1, IL‑6 and IL‑8 due to tumor necrosis factor‑α (TNF‑α) and interferon‑γ (IFN‑γ) in HaCaT cells. TNF‑α and IFN‑γ suppressed the expression of skin barrier proteins, including filaggrin, involucrin and loricrin. By contrast, arazyme increased the expression of filaggrin, involucrin and loricrin. These results may contribute to the development of a therapeutic drug for the treatment of allergic diseases, including atopic dermatitis.
authors.affiliation: Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon, Chungnam 301‑746, Republic of Korea.
authors.forename: In Sik
authors.initials: IS
authors.lastname: Kim
authors.forename: Mi Jin
authors.initials: MJ
authors.lastname: Kim
authors.forename: Dong-Ha
authors.initials: DH
authors.lastname: Shin
authors.forename: Kwang-Hee
authors.initials: KH
authors.lastname: Son
authors.forename: Ho-Yong
authors.initials: HY
authors.lastname: Park
authors.forename: Ji-Sook
authors.initials: JS
authors.lastname: Lee
mesh_terms: D001426:Bacterial Proteins / Q000302:isolation & purification / Q000494:pharmacology*; D002460:Cell Line; D018932:Chemokine CCL2 / Q000096:biosynthesis; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D004755:Enterobacteriaceae / Q000378:metabolism; D004804:Eosinophils / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000091344:Filaggrin Proteins; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis; D007381:Intermediate Filament Proteins / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D045726:Metalloproteases / Q000302:isolation & purification / Q000494:pharmacology*; D009000:Monocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D011498:Protein Precursors / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D001426:Bacterial Proteins; D018932:Chemokine CCL2; D016207:Cytokines; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D016209:Interleukin-8; D007381:Intermediate Filament Proteins; D008565:Membrane Proteins; D011498:Protein Precursors; C064554:loricrin; C032253:involucrin; D045726:Metalloproteases