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Extracellular Signal-Related Kinase (ERK) and p38 Mitogen-Activated Protein (MAP) Kinases Differentially Regulate the Lipopolysaccharide-Mediated Induction of Inducible Nitric Oxide Synthase and IL-12 in Macrophages:LeishmaniaPhosphoglycans Subvert Macrophage IL-12 Production by Targeting ERK MAP Kinase

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Exaggerated Human Monocyte IL-10 Concomitant to Minimal TNF-α Induction by Heat-Shock Protein 27 (Hsp27) Suggests Hsp27 Is Primarily an Antiinflammatory Stimulus

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Differential Induction of Endotoxin Tolerance by Lipopolysaccharides Derived from Porphyromonas gingivalis and Escherichia coli

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Cutting Edge: Myeloid Differentiation Factor 88 Deficiency Improves Resistance Against Sepsis Caused by Polymicrobial Infection

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Dependence of Bacterial Protein Adhesins on Toll-Like Receptors for Proinflammatory Cytokine Induction

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Porphyromonas gingivalisLipopolysaccharide Is Both Agonist and Antagonist for p38 Mitogen-Activated Protein Kinase Activation

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IL-12 Up-Regulates CD40 Ligand (CD154) Expression on Human T Cells

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The lipid A moiety of Porphyromonas gingivalis lipopolysaccharide specifically mediates the activation of C3H/HeJ mice.

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Gram-Positive and Gram-Negative Bacteria Do Not Trigger Monocytic Cytokine Production through Similar Intracellular Pathways

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Stimulation of Splenocytes in C3H/HeJ Mice with Porphyromonas gingivalis Lipid A in Comparison with Enterobacterial Lipid A

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The p38 mitogen-activated protein kinases can have opposing roles in the antigen-dependent or endotoxin-stimulated production of IL-12 and IFN-γ

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Splenic B-cell activation in lipopolysaccharide-non-responsive C3H/HeJ mice by lipopolysaccharide ofPorphyromonas gingivalis

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Lipopolysaccharides (LPS) of Oral Black-Pigmented Bacteria Induce Tumor Necrosis Factor Production by LPS-Refractory C3H/HeJ Macrophages in a Way Different from That of Salmonella LPS

1999 • 12 citations