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or IL-1ß on cellular signaling and mediator production
* Departments of Physiology and Neuroscience and
Pharmacology and Medicine, Medical University of South Carolina, Charleston, and
Institute of Pharmacology, Medical University of Messina, Italy
Correspondence: Prof. James A. Cook, Dept. of Physiology and Neuroscience, 167 Ashley Ave., Suite 617 Storm Eye Institute, Charleston, SC 29425. E-mail: cookja{at}musc.edu
Abstract: Endotoxin [lipopolysaccharide (LPS)] tolerance
suppresses macrophage/monocyte proinflammatory-mediator production.
This phenomenon also confers cross-tolerance to other stimuli including
tumor necrosis factor (TNF) 
and interleukin (IL)-1ß.
Post-receptor convergence of signal transduction pathways might occur
after LPS, IL-1ß, and TNF- stimulation. Therefore, it was
hypothesized that down-regulation of common signaling molecules induces
cross-tolerance among these stimuli. LPS tolerance and cross-tolerance
were examined in THP-1 cells. Phosphorylation of MAP kinases and
degradation of inhibitor 
B (IB) DNA binding of nuclear
factor-B (NF-B), and mediator production were examined. In naive
cells, LPS, TNF-, and IL-1ß induced IB degradation, kinase
phosphorylation, and NF-B DNA binding. LPS stimulation induced
production of TNF- or TxB2 and degradation of IRAK.
However, neither TNF- nor IL-1ß induced IRAK degradation or
stimulated TNF- or TxB2 production in naive cells.
Pretreatment with each stimulus induced homologous tolerance to
restimulation with the same agonist. LPS tolerance also suppressed
LPS-induced TxB2 and TNF- production. LPS
pretreatment induced cross-tolerance to TNF- or IL-1ß stimulation.
Pretreatment with TNF- induced cross-tolerance to LPS-induced
signaling events and TxB2 production. Although pretreatment
with IL-1ß did not induce cross-tolerance to LPS-induced signaling
events, it strongly inhibited LPS TNF- and TxB2
production. These data demonstrate that IL-1ß induces cross-tolerance
to LPS-induced mediator production without suppressing LPS-induced
signaling to MAP kinases or NF-B activation.
Key Words: macrophage/monocyte • signal transduction • phosphorylation • MAP kinases
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