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Soluble ICAM-1 (sICAM-1) provokes PMN elastase release
C C Barnett1, E E Moore, F A Moore
1Department of Surgery, Denver General Hospital and the University of Colorado Health Sciences Center, USA.
The Journal of Surgical Research
|June 1, 1996
Summary
Soluble intercellular adhesion molecule-1 (sICAM-1) significantly increases neutrophil elastase release in vitro. This finding suggests a potential mechanism linking sICAM-1 to the development of multiple organ failure after injury.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Elevated soluble intercellular adhesion molecule-1 (sICAM-1) levels are linked to post-injury multiple organ failure.
- The precise mechanism by which sICAM-1 contributes to organ injury is not fully understood.
- Neutrophil (PMN) activation, involving elastase and superoxide release, is implicated in inflammatory processes and organ damage.
Purpose of the Study:
- To investigate the hypothesis that sICAM-1 augments distant organ injury by affecting neutrophils.
- To examine the effect of sICAM-1 on neutrophil elastase and superoxide production in vitro.
Main Methods:
- Soluble ICAM-1 was isolated from transfected Chinese Hamster Ovarian (CHO) cells.
- Neutrophils were incubated with sICAM-1, and elastase activity was measured using a specific substrate.
- Superoxide production was quantified by measuring ferricytochrome C reduction.
Main Results:
- Incubation with sICAM-1 significantly increased neutrophil elastase release compared to controls.
- The elastase release induced by sICAM-1 was comparable to that of PMA-activated neutrophils.
- sICAM-1 alone did not stimulate spontaneous neutrophil superoxide production.
Conclusions:
- Soluble ICAM-1 directly stimulates neutrophil elastase release in an in vitro setting.
- This action of sICAM-1 on neutrophils may represent a key mechanism in the pathogenesis of post-injury multiple organ failure.