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LPS pretreatment reprograms macrophage LPS‐stimulated TNF and IL‐1 release without protein tyrosine kinase activation
Author(s) -
West Michael A.,
Bennett Terriel,
Seatter Susan C.,
Clair Laurel,
Bellingham Janet
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.61.1.88
Subject(s) - cytokine , biology , tumor necrosis factor alpha , tyrosine kinase , macrophage , microbiology and biotechnology , cancer research , signal transduction , immunology , biochemistry , in vitro
Pretreatment of macrophages with low‐dose endotoxin (LPS p ) profoundly alters cytokine release in response to subsequent LPS a activation. These qualitative and quantitative alterations in cytokine release have been termed macrophage reprogramming. Macrophage activation by LPS is thought to occur via a mechanism involving an early protein tyrosine kinase (PTK) phosphorylation step. PTK inhibition with genistein or herbimycin A blocks LPS a ‐stimulated secretion of tumor necrosis factor (TNF) and interleukin‐1 (IL‐1). In this study we investigated whether a PTK pathway participates in LPS p pretreatment reprogramming. We show that LPSp pretreatment inhibited TNF and augmented IL‐1 release in response to subsequent LPS a stimulation. Blockade of PTK activation pathways during the interval when macrophages were exposed to LPSp prevented mitogen‐activated protein kinase phosphorylation, as well as LPS p ‐stimulated release of TNF and IL‐1, but did not block LPS p reprogramming effects. We conclude that LPS p pretreatment reprogramming of macrophage cytokine production does not require PTK activation. J. Leukoc. Biol . 61: 88–95; 1997.