ST2 protein induced by inflammatory stimuli can modulate acute lung inflammation

被引：91
作者：
Oshikawa, K
Yanagisawa, K
Tominaga, S
Sugiyama, Y
机构：
[1] Jichi Med Sch, Dept Med, Div Pulm Med, Kawachi, Tochigi 3290498, Japan
[2] Jichi Med Sch, Dept Biochem, Kawachi, Tochigi 3290498, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2002年 / 299卷 / 01期
关键词：
acute lung injury; alveolar macrophage; lipopolysaccharide; proinflammatory cytokine; ST2; T-lymphocyte;
D O I：
10.1016/S0006-291X(02)02578-0
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We have investigated gene and protein expression of ST2/ST2L in a murine alveolar macrophage (AM) cell line, MH-S, reacting to inflammatory stimuli in vitro and in the lung tissue of an acute lung injury model in vivo. We have also analyzed the effect of soluble ST2 protein on inflammatory response of MH-S cells. Lipopolysaccharide (LPS) and proinflammatory cytokines such as IL-1beta, IL-6, and TNF-alpha induced ST2 mRNA expression in MH-S cells. In an acute lung injury model, protein and mRNA expression levels of ST2 increased to the maximal level at 24-72 h after the LPS challenge. Furthermore, pretreatment with ST2 protein significantly reduced the protein production and gene expression of IL-1alpha, IL-6, and TNF-alpha in LPS-stimulated MH-S cells in vitro. These results suggest that increases in endogenous ST2 protein in AM, which is induced by inflammatory stimuli, such as LPS and proinflammatory cytokines, may modulate acute lung inflammation. (C) 2002 Elsevier Science (USA). All rights reserved.
引用
收藏
页码：18 / 24
页数：7
相关论文
共 30 条
[1]   ALTERNATIVE PROMOTER USAGE OF THE FOS-RESPONSIVE GENE FIT-1 GENERATES MESSENGER-RNA ISOFORMS CODING FOR EITHER SECRETED OR MEMBRANE-BOUND PROTEINS RELATED TO THE IL-1 RECEPTOR [J].
BERGERS, G ;
REIKERSTORFER, A ;
BRASELMANN, S ;
GRANINGER, P ;
BUSSLINGER, M .
EMBO JOURNAL, 1994, 13 (05) :1176-1188
[2]   EOSINOPHILIC INFLAMMATION IN ASTHMA [J].
BOUSQUET, J ;
CHANEZ, P ;
LACOSTE, JY ;
BARNEON, G ;
GHAVANIAN, N ;
ENANDER, I ;
VENGE, P ;
AHLSTEDT, S ;
SIMONYLAFONTAINE, J ;
GODARD, P ;
MICHEL, FB .
NEW ENGLAND JOURNAL OF MEDICINE, 1990, 323 (15) :1033-1039
[3]   Neutrophil recruitment and increased permeability during acute lung injury induced by lipopolysaccharide [J].
Chignard, M ;
Balloy, V .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2000, 279 (06) :L1083-L1090
[4]   Crucial role of the interleukin 1 receptor family member T1/ST2 in T helper cell type 2-mediated lung mucosal immune responses [J].
Coyle, AJ ;
Lloyd, C ;
Tian, J ;
Nguyen, T ;
Erikkson, C ;
Wang, L ;
Ottoson, P ;
Persson, P ;
Delaney, T ;
Lehar, S ;
Lin, S ;
Poisson, L ;
Meisel, C ;
Kamradt, T ;
Bjerke, T ;
Levinson, D ;
Gutierrez-Ramos, JC .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 190 (07) :895-902
[5]   Transcriptional mechanisms of acute lung injury [J].
Fan, J ;
Ye, RD ;
Malik, AB .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2001, 281 (05) :L1037-L1050
[6]   CLINICAL RISKS FOR DEVELOPMENT OF THE ACUTE RESPIRATORY-DISTRESS SYNDROME [J].
HUDSON, LD ;
MILBERG, JA ;
ANARDI, D ;
MAUNDER, RJ .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1995, 151 (02) :293-301
[7]   Cutting edge:: Lipopolysaccharide induces physical proximity between CD14 and toll-like receptor 4 (TLR4) prior to nuclear translocation of NF-κB [J].
Jiang, QQ ;
Akashi, S ;
Miyake, K ;
Petty, HR .
JOURNAL OF IMMUNOLOGY, 2000, 165 (07) :3541-3544
[8]   Expression of ST2, an interleukin-1 receptor homologue, is induced by proinflammatory stimuli [J].
Kumar, S ;
Tzimas, MN ;
Griswold, DE ;
Young, PR .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 235 (03) :474-478
[9]   Construction of ELISA system to quantify human ST2 protein in sera of patients [J].
Kuroiwa, K ;
Li, HJ ;
Tago, K ;
Iwahana, H ;
Yanagisawa, K ;
Komatsu, N ;
Oshikawa, K ;
Sugiyama, Y ;
Arai, T ;
Tominaga, SI .
HYBRIDOMA, 2000, 19 (02) :151-159
[10]  
Laskin DL, 2001, J LEUKOCYTE BIOL, V70, P163
123