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Departments of
* Molecular and Experimental Medicine and
Immunology, The Scripps Research Institute, La Jolla, CA 92037; and
La Jolla Institute for Allergy and Immunology, San Diego, CA 92121
Proinflammatory cytokines such as IL-1, TNF, IL-6, and IL-8 are
produced by leukocytes in response to bacteria or bacterial components.
A great deal has been learned during the past few years about the
synthesis and release of proinflammatory cytokines by leukocytes;
however, relatively little is known about the intracellular events that
lead to leukocyte proinflammatory cytokine gene transcription. This
study examined the signal transduction pathway of IL-8 induction by
bacterial LPS. Stimulation of monocytes with LPS rapidly activated
RhoA, and pretreatment of monocytes with a RhoA inhibitor, C3
transferase exoenzyme, effectively blocked LPS-induced IL-8 gene
expression. Overexpression of dominant negative RhoA (T19N) or
IL-1R-associated kinase completely inhibited LPS-stimulated reporter
gene expression. Induction of IL-8 was also inhibited by dominant
negative I
B kinase and myeloid differentiation protein (MyD88).
These results indicate that RhoA and IL-1R-associated kinase are novel
signal transducers for LPS-induced Toll-like receptor 4-mediated
proinflammatory cytokine synthesis in human
monocytes.
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