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Department of Microbiology, Molecular Genetics, and Immunology, University of Kansas Medical Center, Kansas City, KS 66160
We studied the potential role of a cytokine regulatory mechanism(s)
in LPS-dependent reprogramming and modulation of TNF-
and nitric
oxide (NO) responses in mouse peritoneal macrophages. Reciprocal
regulation of TNF- and NO production by LPS-primed and
LPS-stimulated macrophages was found to be dependent on the presence of
soluble secretory products released by the cells during the initial LPS
priming interaction. Pretreatment of naïve macrophages with
different mouse recombinant cytokines such as rIL-10, rIL-12, and
rIFN-
dose dependently and differentially regulated subsequent
LPS-induced production of TNF-, IL-6, and NO by cytokine-primed
cells. Analysis of IL-12 and IL-10 levels present in culture
supernatants of LPS-primed and LPS-stimulated macrophages revealed a
high degree of correlation between the profiles of TNF- and IL-12 as
well as NO and IL-10. Furthermore, LPS priming of macrophages in the
presence of anti-IL-12-neutralizing mAb attenuated TNF-
responses while at the same time up-regulated NO production. In
contrast, neutralization of endogenous IL-10 with anti-IL-10 mAb
resulted in considerable TNF- response at LPS priming doses under
conditions that would otherwise strongly inhibit TNF- production. We
also found that the initial LPS priming of naïve macrophages
differentially and dose dependently regulates expression of mRNAs for
IL-10, IL-12, and IFN- in LPS-primed macrophages. Collectively, our
data provide experimental support for the hypothesis that a cytokine
regulatory network, most probably autocrine, tightly controls the
reciprocal modulation of TNF- and NO responses in LPS-primed
macrophages.
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