The novel role of platelet-activating factor in protecting mice against lipopolysaccharide-induced endotoxic shock.
BACKGROUND
Platelet-activating factor (PAF) has been long believed to be associated with many pathophysiological processes during septic shock. Here we present novel activities for PAF in protecting mice against LPS-mediated endotoxic shock.


RESULTS
In vivo PAF treatment immediately after LPS challenge markedly improved the survival rate against mortality from endotoxic shock. Administration of PAF prominently attenuated LPS-induced organ injury, including profound hypotension, excessive polymorphonuclear neutrophil infiltration, and severe multiple organ failure. In addition, PAF treatment protects against LPS-induced lymphocytes apoptosis. These protective effects of PAF was correlated with significantly decreases in the production of the inflammatory mediators such as TNF-alpha, IL-1beta, IL-12, and IFN-gamma, while increasing production of the anti-inflammatory cytokine IL-10 in vivo and in vitro.


CONCLUSIONS
Taken together, these results suggest that PAF may protect mice against endotoxic shock via a complex mechanism involving modulation of inflammatory and anti-inflammatory mediators.
Jeong
Young-Il
YI
Department of Microbiology, College of Natural Science, Pusan National University, Geumjeong-Gu, Busan, Korea.
Jung
In Duk
ID
Lee
Chang-Min
CM
Chang
Jeong Hyun
JH
Chun
Sung Hak
SH
Noh
Kyung Tae
KT
Jeong
Soo Kyung
SK
Shin
Yong Kyoo
YK
Lee
Won Suk
WS
Kang
Mi Sun
MS
Lee
Sang-Yull
SY
Lee
Jae-Dong
JD
Park
Yeong-Min
YM
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D008214:Lymphocytes / Q000187:drug effects; D051379:Mice; D010972:Platelet Activating Factor / Q000008:administration & dosage / Q000494:pharmacology*; D012772:Shock, Septic / Q000378:metabolism / Q000517:prevention & control*
D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D010972:Platelet Activating Factor