Format

Send to

Choose Destination
See comment in PubMed Commons below
Mol Med Rep. 2013 Aug;8(2):551-6. doi: 10.3892/mmr.2013.1520. Epub 2013 Jun 13.

Arazyme inhibits cytokine expression and upregulates skin barrier protein expression.

Author information

1
Department of Biomedical Laboratory Science, School of Medicine, Eulji University, Daejeon, Chungnam 301‑746, Republic of Korea.

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.

PMID:
23764888
DOI:
10.3892/mmr.2013.1520
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Spandidos Publications
    Loading ...
    Support Center