Complement-dependent accumulation and degradation of platelets in the lung and liver induced by injection of lipopolysaccharides

被引:62
作者
Shibazaki, M
Kawabata, Y
Yokochi, T
Nishida, A
Takada, H
Endo, Y
机构
[1] Tohoku Univ, Sch Dent, Dept Pharmacol, Aoba Ku, Sendai, Miyagi 980, Japan
[2] Tohoku Univ, Sch Dent, Dept Immunol & Microbiol, Sendai, Miyagi 980, Japan
[3] Tohoku Univ, Fac Agr, Dept Anim Sci, Sendai, Miyagi 980, Japan
[4] Kagoshima Univ, Sch Dent, Dept Dent Radiol, Kagoshima 890, Japan
[5] Aichi Med Univ, Dept Microbiol & Immunol, Nagakute, Aichi 48011, Japan
关键词
D O I
10.1128/IAI.67.10.5186-5191.1999
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We found unique behaviors among platelets within a few minutes of the intravenous injection of lipopolysaccharide (LPS) into mice. Platelets accumulated primarily in the liver at lower doses of LPS, but at higher doses they accumulated largely in the lungs, When the platelets accumulated in these organs were degraded, there was a rapid anaphylactoid shock The platelet response depended on the strain of mouse and on the source of LPS, Of various LPSs tested, the LPS from the smooth type of Klebsiella O3 (KO3-S LPS) was the most potent at inducing the platelet response and shock K-76 monocarboxylic acid, an inhibitor of complement (C5, effectively prevented the KO3-S LPS-induced degradation (but not accumulation) of platelets and the ensuing rapid shock in BALB/c mice. Moreover, in DBA/2 mice which are deficient in complement C5), platelets accumulated in the lungs and liver in response to KO3-S LPS hut soon returned to the circulation without degradation, and there was no rapid shock. The LPS from the rough type of KO3 induced an accumulation of platelets in the liver and lungs but not a degradation of platelets, On the basis of these results and those reported by other investigators, we propose that in the platelet response to LPS, the lectin pathway to form C3 convertase from C4 and C2 is invoiced in the rapid accumulation of platelets in the liver and lungs and that the pathway from C5 to C9 is involved in the destruction of platelets and the consequent anaphylactoid shock.
引用
收藏
页码:5186 / 5191
页数:6
相关论文
共 32 条
[1]  
Boivin A, 1933, CR SEANC SOC BIOL PA, V113, P490
[2]   BEHAVIOR OF COMPLEMENT AND PLATELETS IN LETHAL ENDOTOXIN-SHOCK IN RABBITS [J].
BROWN, DL ;
LACHMANN, PJ .
INTERNATIONAL ARCHIVES OF ALLERGY AND APPLIED IMMUNOLOGY, 1973, 45 (1-2) :193-205
[3]  
CARNER R, 1974, BRIT J HAEMATOL, V28, P393
[4]   DISTRIBUTION INHERITANCE + PROPERTIES OF ANTIGEN MUBI + ITS RELATION TO HEMOLYTIC COMPLEMENT [J].
CINADER, B ;
WARDLAW, AC ;
DUBISKI, S .
JOURNAL OF EXPERIMENTAL MEDICINE, 1964, 120 (05) :897-&
[5]  
DAVIS PB, 1961, P SOC EXP BIOL MED, V108, P774
[6]   IMMEDIATE EFFECTS OF INTRAVENOUS ENDOTOXIN ON SEROTONIN CONCENTRATIONS AND BLOOD PLATELETS [J].
DAVIS, RB ;
MEEKER, WR ;
MCQUARRIE, DG .
CIRCULATION RESEARCH, 1960, 8 (01) :234-239
[7]   Contrasting effects of lipopolysaccharides (Endotoxins) from oral black-pigmented bacteria and Enterobacteriaceae on platelets, a major source of serotonin, and on histamine-forming enzyme in mice [J].
Endo, Y ;
Shibazaki, M ;
Nakamura, M ;
Takada, H .
JOURNAL OF INFECTIOUS DISEASES, 1997, 175 (06) :1404-1412
[8]   ACTIVE TRANSLOCATION OF PLATELETS INTO SINUSOIDAL AND DISSE SPACES IN THE LIVER IN RESPONSE TO LIPOPOLYSACCHARIDES, INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR [J].
ENDO, Y ;
NAKAMURA, M .
GENERAL PHARMACOLOGY-THE VASCULAR SYSTEM, 1993, 24 (05) :1039-1053
[9]   THE EFFECT OF LIPOPOLYSACCHARIDE, INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR ON THE HEPATIC ACCUMULATION OF 5-HYDROXYTRYPTAMINE AND PLATELETS IN THE MOUSE [J].
ENDO, Y ;
NAKAMURA, M .
BRITISH JOURNAL OF PHARMACOLOGY, 1992, 105 (03) :613-619
[10]   A NEW METHOD FOR EXTRACTION OF R-LIPOPOLYSACCHARIDES [J].
GALANOS, C ;
LUDERITZ, O ;
WESTPHAL, O .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1969, 9 (02) :245-&