Rapid pulmonary expression of acute-phase reactants after local lipopolysaccharide exposure in mice is followed by an interleukin-6 mediated systemic acute-phase response

被引:21
作者
Vernooy, JHJ
Reynaert, N
Cloots, RHE
Haegens, A
de Vries, B
Dentener, MA
Buurman, WA
Wouters, EFM
机构
[1] Univ Hosp Maastricht, Dept Resp Med, NUTRIM, NL-6202 AZ Maastricht, Netherlands
[2] Univ Hosp Maastricht, Dept Gen Surg, NUTRIM, Maastricht, Netherlands
关键词
acute-phase response; inflammation; innate immunity; lipopolysaccharide; lung;
D O I
10.1080/01902140600611645
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
This study investigated local and systemic innate immune responses in lipopolysaccharide (LPS)-induced lung inflammation in mice. Intratracheal LPS exposure resulted in increased pulmonary mRNA expression for acute-phase reactants (APRs) alpha(1)-antitrypsin (alpha(1)-AT), alpha(1)-acid glycoprotein (AGP), and LPS-binding protein (LBP) from 4 hours post exposure. Although pulmonary serum amyloid P component (SAP) mRNA was not, increased, systemic levels of SAP AGP and LBP were elevated from 24 hours post exposure. Systemic APRs increase was associated with hepatic mRNA expression. As in vivo neutralization of interleukin (IL)-6, but not tumor necrosis factor (TNF)-alpha, fully ablated hepatic APR mRNA expression, IL-6 may act as signaling molecule between lung and, liver. In conclusion, pulmonary LPS exposure induced rapid APR expression in lung, which precedes IL-6-mediated systemic elevation of APRs associated with hepatic APRs expression.
引用
收藏
页码:855 / 871
页数:17
相关论文
共 53 条
[1]   EFFECT OF ANTITUMOR NECROSIS FACTOR TREATMENT ON CIRCULATING TUMOR-NECROSIS-FACTOR LEVELS AND MORTALITY AFTER SURGERY IN JAUNDICED MICE [J].
BEMELMANS, MHA ;
GOUMA, DJ ;
GREVE, JW ;
BUURMAN, WA .
BRITISH JOURNAL OF SURGERY, 1993, 80 (08) :1055-1058
[2]  
BEMELMANS MHA, 1993, J IMMUNOL, V151, P5554
[3]  
Bopst M, 1998, EUR J IMMUNOL, V28, P4130, DOI 10.1002/(SICI)1521-4141(199812)28:12<4130::AID-IMMU4130>3.0.CO
[4]  
2-W
[5]   PREVALENCE OF TRIANTENNARY AND TETRAANTENNARY GLYCANS OF HUMAN ALPHA-1-ACID GLYCOPROTEIN IN RELEASE OF MACROPHAGE INHIBITOR OF INTERLEUKIN-1 ACTIVITY [J].
BORIES, PN ;
FEGER, J ;
BENBERNOU, N ;
ROUZEAU, JD ;
AGNERAY, J ;
DURAND, G .
INFLAMMATION, 1990, 14 (03) :315-323
[6]   ALPHA-1-ACID GLYCOPROTEIN POTENTIATES LIPOPOLYSACCHARIDE-INDUCED SECRETION OF INTERLEUKIN-1-BETA, INTERLEUKIN-6 AND TUMOR-NECROSIS-FACTOR-ALPHA BY HUMAN MONOCYTES AND ALVEOLAR AND PERITONEAL-MACROPHAGES [J].
BOUTTEN, A ;
DEHOUX, M ;
DESCHENES, M ;
ROUZEAU, JD ;
BORIES, PN ;
DURAND, G .
EUROPEAN JOURNAL OF IMMUNOLOGY, 1992, 22 (10) :2687-2695
[7]   INHIBITION OF NEUTROPHIL SUPEROXIDE PRODUCTION BY HUMAN PLASMA ALPHA-1-ANTITRYPSIN [J].
BUCURENCI, N ;
BLAKE, DR ;
CHIDWICK, K ;
WINYARD, PG .
FEBS LETTERS, 1992, 300 (01) :21-24
[8]   THE EFFECTS OF INHALATION OF GRAIN DUST EXTRACT AND ENDOTOXIN ON UPPER AND LOWER AIRWAYS [J].
CLAPP, WD ;
THORNE, PS ;
FREES, KL ;
ZHANG, XJ ;
LUX, CR ;
SCHWARTZ, DA .
CHEST, 1993, 104 (03) :825-830
[9]  
Crestani B, 1998, J IMMUNOL, V160, P4596
[10]   Functional protection by acute phase proteins α1-acid glycoprotein and α1-antitrypsin against ischemia/reperfusion injury by preventing apoptosis and inflammation [J].
Daemen, MARC ;
Heemskerk, VH ;
van 't Veer, C ;
Denecker, G ;
Wolfs, TGAM ;
Vandenabeele, P ;
Buurman, WA .
CIRCULATION, 2000, 102 (12) :1420-1426