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and IL-10 Formation by Human Macrophages Is Differentially Regulated at the Level of Mitogen-Activated Protein Kinase Activity1
Departments of
*
Immunochemistry and Biochemical Microbiology and
Immunology and Cell Biology, Research Center Borstel, Borstel, Germany
The clinical course of mycobacterial infections is linked to the
capacity of pathogenic strains to modulate the initial
antimycobacterial response of the macrophage. To elucidate some of the
mechanisms involved, we studied early signal transduction events
leading to cytokine formation by human monocyte-derived macrophages
(MDM) in response to clinical isolates of Mycobacterium
avium. TNF-
production induced by M. avium
was inhibited by anti-CD14 mAbs, but not by Abs against the
macrophage mannose receptor. Analysis of mitogen-activated protein
(MAP) kinase activation (extracellular signal-regulated kinase 1/2,
p38, and c-Jun NH2-terminal kinase) showed a rapid
phosphorylation of all three subfamilies in response to M.
avium, which was inhibited by anti-CD14 Abs. Using highly
specific inhibitors of p38 (SB203580) and MAP kinase kinase-1
(PD98059), we found that activation of the extracellular
signal-regulated kinase pathway, but not of p38, was essential for the
M. avium-induced TNF- formation. In contrast, IL-10
production was abrogated by the p38 inhibitor, but not by the MAP
kinase kinase-1 inhibitor. In conclusion, M.
avium-induced secretion of TNF- and IL-10 by human
macrophages is differentially regulated at the level of MAP kinase
activity.
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