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Vol. 55, Issue 4, 658-667, April 1999
B Degradation and
Reduces Microvascular Injury Induced by Lipopolysaccharide in
Multiple Organs
Department of Pharmacology, The University of Illinois, College of
Medicine, Chicago, Illinois
Lipopolysaccharide (LPS) is a key mediator of multiple organ injury
observed in septic shock. The mechanisms responsible for LPS-induced
multiple organ injury remain obscure. In the present study, we tested
the hypothesis that the LPS-induced injury occurs through activation of
the transcription factor, nuclear factor-
B (NF-B). We examined
the effects of inhibiting NF-B activation in vivo in the rat on
LPS-induced: 1) gene and protein expression of the cytokine-inducible
neutrophil chemoattractant (CINC) and intercellular adhesion molecule-1
(ICAM-1); b) neutrophil influx into lungs, heart, and liver; and c)
increase in microvascular permeability induced by LPS in these organs.
LPS (8 mg/kg, i.v.) challenge of rats activated NF-B and induced
CINC and ICAM-1 mRNA and protein expression. Pretreatment of rats with
pyrrolidine dithiocarbamate (50, 100, and 200 mg/kg, i.p.), an
inhibitor of NF-B activation, prevented LPS-induced I-B
degradation and the resultant NF-B activation and inhibited, in a
dose-related manner, the LPS-induced CINC and ICAM-1 mRNA and protein
expression. Pyrrolidine dithiocarbamate also markedly reduced the
LPS-induced tissue myeloperoxidase activity (an indicator of tissue
neutrophil retention) and the LPS-induced increase in microvascular
permeability in these organs. These results demonstrate that NF-B
activation is an important in vivo mechanism mediating LPS-induced CINC
and ICAM-1 expression, as well as neutrophil recruitment, and the subsequent organ injury. Thus, inhibition of NF-B activation may be
an important strategy for the treatment of sepsis-induced multiple
organ injury.
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