Expression of interleukin-17F in a mouse model of allergic asthma

被引:40
作者
Suzuki, Shintaro
Kokubu, Fumio
Kawaguchi, Mio
Homma, Tetsuya
Odaka, Miho
Watanabe, Shin
Ieki, Koshi
Matsukura, Satoshi
Kurokawa, Masatsugu
Takeuchi, Hiroko
Sasaki, Yoshiko
Huang, Shau-Ku
Adachi, Mitsuru
Ota, Hidekazu
机构
[1] Showa Univ, Sch Med, Dept Internal Med 1, Shinagawa Ku, Tokyo 1428666, Japan
[2] Showa Univ, Sch Med, Dept Pathol 2, Tokyo 1428666, Japan
[3] Showa Univ, Fujigaoka Hosp, Dept Resp Med, Kanagawa, Japan
[4] Johns Hopkins Univ, Ctr Asthma & Allergy, Baltimore, MD 21224 USA
关键词
bronchial asthma; glucocorticoids; interleukin-17F;
D O I
10.1159/000101413
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Interleukin (IL)-17F is a recently discovered cytokine and is derived from a panel of limited cell types, such as activated CD4+ T cells, basophils, and mast cells. IL-17F is known to induce several cytokines and chemokines. However, its involvement in airway inflammation has not been well understood. To this end, the expression of IL-17F and the inhibitory effects of glucocorticoids on its expression in a mouse model of asthma were examined. Methods: Five-week-old BALB/c male mice were sensitized by intraperitoneal injection (i. p.) of ovalbumin (OVA) with alum, and challenged by daily inhalation of aerosolized 1% OVA. 24 h after last challenge (OVA/OVA), the expression of IL-17F was examined in lung tissues by immunohistochemistry and reverse-transcription polymerase chain reaction. Control mice were sensitized and challenged with saline (Sham/Sham). In addition, a group of OVA-sensitized mice received i. p. injection of water-soluble dexamethasone (DEX) in saline 1 h before OVA challenge (OVA/DEX). Results: In sham-challenged mice, IL-17F was not expressed in the lungs, while, in contrast, IL-17F was predominantly expressed in bronchial epithelial cells in addition to the infiltrating inflammatory cells in OVA/OVA mice. Further, the expression of IL-17 F was significantly attenuated by the treatment of mice with DEX. Conclusion: These results suggest that bronchial epithelium-derived IL-17F may represent a new pharmacological target for glucocorticoids and may play a role in allergic asthma. Copyright (C) 2007 S. Karger AG, Basel.
引用
收藏
页码:89 / 94
页数:6
相关论文
共 25 条
[1]  
ALEXANDRE T, 2000, AM J PHYSIOL, V279, pL1120
[2]   Corticosteroid effects on cell signalling [J].
Barnes, PJ .
EUROPEAN RESPIRATORY JOURNAL, 2006, 27 (02) :413-426
[3]   Tumour necrosis factor-α stimulates dehydroepiandrosterone metabolism in human fibroblast-like synoviocytes:: a role for nuclear factor-κB and activator protein-1 in the regulation of expression of cytochrome p450 enzyme 7b [J].
Dulos, J ;
Kaptein, A ;
Kavelaars, A ;
Heijnen, C ;
Boots, A .
ARTHRITIS RESEARCH & THERAPY, 2005, 7 (06) :R1271-R1280
[4]   New IL-17 family members promote Th1 or Th2 responses in the lung: In vivo function of the novel cytokine IL-25 [J].
Hurst, SD ;
Muchamuel, T ;
Gorman, DM ;
Gilbert, JM ;
Clifford, T ;
Kwan, S ;
Menon, S ;
Seymour, B ;
Jackson, C ;
Kung, TT ;
Brieland, JK ;
Zurawski, SM ;
Chapman, RW ;
Zurawski, G ;
Coffman, RL .
JOURNAL OF IMMUNOLOGY, 2002, 169 (01) :443-453
[5]   IL-17s adopt a cystine knot fold: structure and activity of a novel cytokine, IL-17F, and implications for receptor binding [J].
Hymowitz, SG ;
Filvaroff, EH ;
Yin, JP ;
Lee, J ;
Cai, LP ;
Risser, P ;
Maruoka, M ;
Mao, WG ;
Foster, J ;
Kelley, RF ;
Pan, GH ;
Gurney, AL ;
de Vos, AM ;
Starovasnik, MA .
EMBO JOURNAL, 2001, 20 (19) :5332-5341
[6]   IL-17F sequence variant (His161Arg) is associated with protection against asthma and antagonizes wild-type IL-17F activity [J].
Kawaguchi, M ;
Takahashi, D ;
Hizawa, N ;
Suzuki, S ;
Matsukura, S ;
Kokubu, F ;
Maeda, Y ;
Fukui, Y ;
Konno, S ;
Huang, SK ;
Nishimura, M ;
Adachi, M .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2006, 117 (04) :795-801
[7]   IL-17 cytokine family [J].
Kawaguchi, M ;
Adachi, M ;
Oda, N ;
Kokubu, F ;
Huang, SK .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2004, 114 (06) :1265-1274
[8]   Induction of granulocyte-macrophage colony-stimulating factor by a new cytokine, ML-1 (IL-17F), via Raf I-MEK-ERK pathway [J].
Kawaguchi, M ;
Kokubu, F ;
Odaka, M ;
Watanabe, S ;
Suzuki, S ;
Leki, K ;
Matsukura, S ;
Kurokawa, M ;
Adachi, M ;
Huang, SK .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2004, 114 (02) :444-450
[9]   Induction of C-X-C chemokines, growth-related oncogene α expression, and epithelial cell-derived neutrophil-activating protein-78 by ML-1 (interleukin-17F) involves activation of Raf1-mitogen-activated protein kinase kinase-extracellular signal-regulated kinase 1/2 pathway [J].
Kawaguchi, M ;
Kokubu, F ;
Matsukura, S ;
Ieki, K ;
Odaka, M ;
Watanabe, S ;
Suzuki, S ;
Adachi, M ;
Huang, SK .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2003, 307 (03) :1213-1220
[10]   Activation of extracellular signal-regulated kinase (ERK)1/2, but not p38 and c-Jun N-terminal kinase, is involved in signaling of a novel cytokine, ML-1 [J].
Kawaguchi, M ;
Onuchic, LF ;
Huang, SK .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (18) :15229-15232