Expression of intercellular adhesion molecule-1 (ICAM-1) in choriodecidua with labour and delivery at term and preterm

1999 ◽  
Vol 11 (5) ◽  
pp. 255 ◽  
Author(s):  
Keith W. Marvin ◽  
Jeffrey A. Keelan ◽  
Timothy A. Sato ◽  
Matthew A. G. Coleman ◽  
Lesley M. E. McCowan ◽  
...  

To evaluate the association between intercellular adhesion molecule-1 (ICAM-1) in the chorio-decidua and preterm labour and delivery, ICAM-1 mRNA abundance was assessed by northern analysis, and protein levels by ELISA, in samples of this tissue after term and preterm delivery. The median ICAM-1 mRNA expression following preterm delivery (PTD) was 4.8 and 3.8 times (P<0.05), respectively, those following elective Caesarean section prior to labour at term (CST) and following vaginal delivery after spontaneous labour at term (SLT). The concentration of ICAM-1 protein in the PTD samples was 2.2 and 3.0 times (P<0.05) those in CST and SLT samples, respectively. The differences between the term groups were not significant. The results were substantially the same when a preterm spontaneous labour (PTL) subgroup, exclusive of deliveries complicated by pre-eclampsia or intrauterine growth restriction, was compared with the term groups. Choriodecidual ICAM-1 mRNA expression, but not ICAM-1 protein concentration, significantly correlated to the degree of leukocyte infiltration of the PTD gestational membranes. Neither correlated significantly to clinical indications of intrauterine or neonatal infection. These findings indicate that ICAM-1 is expressed by the human choriodecidua and that this expression is elevated with preterm labour and delivery, particularly with increased leukocyte infiltration.

2004 ◽  
Vol 29 (3) ◽  
pp. 228-232 ◽  
Author(s):  
N. ISOGAI ◽  
H. TANAKA ◽  
S. ASAMURA

This study was undertaken to characterize the relative degrees of arterial and venous trauma after graded avulsion injuries. Rat femoral arteries and veins were subjected to reproducible avulsion injuries using forces of between 60 and 220 g. Thrombotic occlusion occurred at lower avulsion forces in veins than in arteries. Histologic and scanning electron microscopic analysis indicated increased endothelial disruption and exposed elastic lamina with increasing avulsion force in both vessels, but more prominently in arteries. Intercellular adhesion molecule-1 (ICAM-1) mRNA expression was evident at 3 and 6 hours after avulsion injury in veins, but only with higher avulsion force injuries in arteries. ICAM-1 mRNA expression was not found in either vessel before or after this 3 to 6 hour post-injury interval. These results indicate that the amount of avulsion force to which traumatized extremity vessels are subjected has a direct effect on the degree of intimal injury and subsequent thrombosis.


1994 ◽  
Vol 4 (9) ◽  
pp. 1695-1700
Author(s):  
D J Nikolic-Paterson ◽  
H Y Lan ◽  
P A Hill ◽  
J L Vannice ◽  
R C Atkins

Interleukin-1 is a proinflammatory cytokine produced in glomerulonephritis. Blocking the action of interleukin-1 by the administration of the interleukin-1 receptor antagonist (IL-1ra) has been shown to prevent renal function impairment, reduce glomerular injury, inhibit leukocyte infiltration, and suppress tubulointerstitial damage in experimental antiglomerular basement membrane disease. A key mechanism in the entry of leukocytes into the kidney is the interaction between the interleukin-1 inducible intercellular adhesion molecule-1 (ICAM-1; CD54) and lymphocyte function-associated antigen-1 (CD11a/CD18). Therefore, this study investigated whether the inhibition of this mechanism was the means by which IL-1ra suppressed leukocyte infiltration in rat accelerated antiglomerular basement membrane glomerulonephritis. Disease was induced in two groups of six rats; animals were treated by constant sc infusion of recombinant human IL-1ra or saline from the initiation of disease until being euthanized 14 days later. In saline-treated animals, there was marked up-regulation of ICAM-1 in the glomerulus and interstitium, In which was associated with leukocyte infiltration. In particular, focal accumulation of CD11a+ and CD18+ cells was apparent in areas of tubulointerstitial damage exhibiting intense ICAM-1 expression. IL-1ra treatment partially reduced glomerular ICAM-1 expression and leukocyte infiltration. However, IL-1ra treatment resulted in a dramatic inhibition of interstitial ICAM-1 expression, interstitial leukocyte infiltration, and tubulointerstitial damage. In conclusion, this study has shown that interleukin-1 is a major inducer of ICAM-1 expression within the renal tubulo-interstitium--a process associated with focal leukocyte infiltration and tubulointerstitial damage.(ABSTRACT TRUNCATED AT 250 WORDS)


Placenta ◽  
2000 ◽  
Vol 21 (1) ◽  
pp. 115-121 ◽  
Author(s):  
K.W. Marvin ◽  
J.A. Keelan ◽  
T.A. Sato ◽  
M.A.G. Coleman ◽  
L.M.E. Mccowan ◽  
...  

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