Loading…
Human serum amyloid P component attenuates the bacterial lipopolysaccharide-induced increase in blood–brain barrier permeability in mice
Endotoxin challenge leads to septic shock, multi-organ failure and death in mice. Permeability of the blood–brain barrier (BBB) is increased by endotoxemia. Serum amyloid P component (SAP) is a lipopolysaccharide (LPS)-binding protein that can modulate the host reactions during infections. It is con...
Saved in:
Published in: | Neuroscience letters 2003-11, Vol.352 (1), p.57-60 |
---|---|
Main Authors: | , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Endotoxin challenge leads to septic shock, multi-organ failure and death in mice. Permeability of the blood–brain barrier (BBB) is increased by endotoxemia. Serum amyloid P component (SAP) is a lipopolysaccharide (LPS)-binding protein that can modulate the host reactions during infections. It is controversial whether SAP can protect from LPS toxicity in vivo or not. We have tested the effect of human SAP on BBB permeability of
Salmonella typhimurium LPS-injected mice. The animals showed signs of sickness behaviour including immobility, anorexia, and diarrhoea. Intraperitoneally administered LPS increased the BBB permeability for sodium fluorescein for about 4-fold, and for albumin for more than 2-fold in brain cortex. SAP, given intravenously, had no effect on basal BBB permeability for albumin, although it decreased sodium fluorescein extravasation to brain tissue. In LPS-treated mice, SAP administration alleviated the symptoms of septic shock, and significantly inhibited the enhanced BBB permeability for both tracers. Our data indicate that human SAP may counteract the toxic effects of LPS during septic shock. |
---|---|
ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2003.08.028 |