Page 27 - M. Immunology

Therapeutic and anti-inflammatory effect of Bleomycin induced Systemic
sclerosis using W-peptide
Gyu Tae Park*, Yang Woo Kwon, Young-cheol Song, Jae Ho Kim

Medical Research Center for Ischemic Tissue Regeneration & Medical Research Institute, Department of Physiology, School of Medicine,
Pusan National University, Yang san 626-870, Republic of Korea
BACKGROUND METHODS

Systemic sclerosis is an autoimmune disease that affects For making of sclerosis model, Wild Type and FPR2
multiple organs. It is caused by irregulated immune function Knock out mice were administrated bleomycin to
and enlargement of connective tissue. Abnormal inflammatory subcutaneous area for 3 weeks, and co-injected with W-
activation is induce fibrosis, such as fibroblast activation, and peptide for therapy of scleroderma. For check of fibrosis,
collagen production. Formyl Peptide Receptor-2(FPR2) is a G- We determined dermal thickness, and collagen density
protein coupled receptor that expressed in Neutrophil, and using Masson trichrome staining and hydroxyproline
Monocyte. It is regulate inflammatory cell apoptosis, and assay. For check of regulation of fibroblast activation,
inflammatory cytokine expression. In previous reports was mouse tissue were stained to alpha SMA, a myofibroblast
conducted to investigate the effect of FPR2 activation in marker, and Vimentin, a fibroblast number, and counted
sclerosis. α-sma positive and vimentin positive cell number. For
AIM check of inflammation, skin tissue were stained CD68, a
marker of inflammatory cell. And inflammatory cytokine
we conducted an experiment to determine whether FPR2 level in mice sera was determinated through ELISA
activation through W-peptide, a agonistic peptide of FPR2, has assay.
a therapeutic effect of Sclerosis disease.
RESULTS
Figure 1 Figure 2 Figure 3

Figure 4 Figure 5 Figure 6

W-peptide has been shown to have a curative effect on scleroderma through reduction of skin thickness and collagen
accumulation, and can control fibroblast activation and inflammatory response(Fig 1-3). However, in the FPR2 KO condition, the
effect of W-pepdie is down regulated. (Fig 4-6) through this, it was confirmed that W-peptide treats scleroderma through the
action of FPR2.
CONCLUSION REFERENCES Contact information

W peptides inhibit activation of Fibro- 1.Varga J, Abraham D. J Clin Invest. Address : Department of Physiology,
blast and thus collagen accumulation 2007;117(3):557-67.. School of Medicine, Pusan National
and connective tissue hypertrophy by University, Yang san 626-870, Kyeong
regulating immune cell infiltration and 2.Ye RD, Boulay F Pharmacol Rev. Sang Nam-Do, Republic of Korea
cytokine expression in a scleroderma 2009;61(2):119-61 Telephone : +82)051-510-8070
model induced by Bleomycin. This 3.Rossi FW, Montuori N. Oncotarget.
mechanism prevents FPR2 knockout 2015;6(22):18736-7. Mobile : +82)010-2828-9184
from treating the FPR2 mechanism E-mail : daramzuy2@naver.com
Which is a major contributor to the 4.Rossi FW. J Immunol.
inhibition of scleroderma. 2015;194(11):5161-73.