The Journal of Experimental Medicine
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Published 3 January 2005. doi:10.1084/jem.20040616
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 1, 73-82
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ARTICLE

 Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness

Hiromasa Inoue1, Reiko Kato2, Satoru Fukuyama1,2, Atsushi Nonami2, Kouji Taniguchi2, Koichiro Matsumoto1, Takako Nakano1, Miyuki Tsuda1, Mikiko Matsumura1, Masato Kubo4, Fumihiko Ishikawa3, Byoung-gon Moon5, Kiyoshi Takatsu5, Yoichi Nakanishi1, and Akihiko Yoshimura2

1 Research Institute for Diseases of the Chest, Graduate School of Medical Sciences
2 Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation
3 The First Department of Internal Medicine, Faculty of Medicine, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan
4 Laboratory for Signal Network, RIKEN Research Center for Allergy and Immunology, Institute of Chemical and Physical Research (RIKEN), Yokohama Institute, Tsurumi, Yokohama, Kanagawa 230-0045, Japan
5 Department of Immunology, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan

CORRESPONDENCE Hiromasa Inoue: inoue{at}kokyu.med.kyushu-u.ac.jp

T helper 2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, play a critical role in allergic asthma. These cytokines transmit signals through the Janus kinase/signal transducer and activator of transcription (STAT) and the Ras–extracellular signal-regulated kinase (ERK) signaling pathways. Although the suppressor of cytokine signaling (SOCS) family proteins have been shown to regulate the STAT pathway, the mechanism regulating the ERK pathway has not been clarified. The Sprouty-related Ena/VASP homology 1–domain-containing protein (Spred)-1 has recently been identified as a negative regulator of growth factor–mediated, Ras-dependent ERK activation. Here, using Spred-1–deficient mice, we demonstrated that Spred-1 negatively regulates allergen-induced airway eosinophilia and hyperresponsiveness, without affecting helper T cell differentiation. Biochemical assays indicate that Spred-1 suppresses IL-5–dependent cell proliferation and ERK activation. These data indicate that Spred-1 negatively controls eosinophil numbers and functions by modulating IL-5 signaling in allergic asthma.

Abbreviations used: AHR, airway hyperresponsiveness; BAL, bronchoalveolar lavage; BMEo, BM–derived eosinophil; EGFP, enhanced GFP; ERK, extracellular signal-regulated kinase; PAS, periodic acid-Schiff; Spred, Sprouty-related EVH1-domain-containing protein.

H. Inoue, R. Kato, and S. Fukuyama contributed equally to this work.


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