1. Differential cytokine response in host defence mechanisms triggered by gram-negative and gram-positive bacteria, and the roles of gabexate mesilate, a synthetic protease inhibitor.
- Author
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Iwadou H, Morimoto Y, Iwagaki H, Sinoura S, Chouda Y, Kodama M, Yoshioka T, Saito S, Yagi T, and Tanaka N
- Subjects
- Antigens, CD immunology, Antigens, CD metabolism, Cells, Cultured, Enterotoxins immunology, Gabexate therapeutic use, Gram-Negative Bacteria immunology, Gram-Negative Bacteria metabolism, Gram-Negative Bacterial Infections drug therapy, Gram-Negative Bacterial Infections immunology, Gram-Positive Bacteria immunology, Gram-Positive Bacteria metabolism, Gram-Positive Bacterial Infections drug therapy, Gram-Positive Bacterial Infections immunology, Humans, Interferon-gamma immunology, Interferon-gamma metabolism, Interleukin 1 Receptor Antagonist Protein, Interleukin-1 immunology, Interleukin-1 metabolism, Interleukin-10 immunology, Interleukin-10 metabolism, Interleukin-18 immunology, Interleukin-2 immunology, Interleukin-2 metabolism, Interleukin-6 immunology, Interleukin-6 metabolism, Leukocytes, Mononuclear cytology, Leukocytes, Mononuclear immunology, Lipopolysaccharides immunology, Membrane Glycoproteins genetics, Membrane Glycoproteins immunology, Membrane Glycoproteins metabolism, NF-kappa B metabolism, Receptors, Cell Surface genetics, Receptors, Cell Surface immunology, Receptors, Cell Surface metabolism, Receptors, Tumor Necrosis Factor immunology, Receptors, Tumor Necrosis Factor metabolism, Receptors, Tumor Necrosis Factor, Type II, Serine Proteinase Inhibitors therapeutic use, Sialoglycoproteins immunology, Sialoglycoproteins metabolism, Signal Transduction physiology, Superantigens immunology, Superantigens pharmacology, Toll-Like Receptor 2, Toll-Like Receptor 4, Toll-Like Receptors, Tumor Necrosis Factor-alpha immunology, Drosophila Proteins, Enterotoxins pharmacology, Gabexate pharmacology, Interleukin-18 metabolism, Leukocytes, Mononuclear drug effects, Lipopolysaccharides pharmacology, Serine Proteinase Inhibitors pharmacology, Tumor Necrosis Factor-alpha metabolism
- Abstract
Bacterial infection results in the production of inflammatory mediators and may be involved in the pathogenesis of sepsis and/or systemic inflammatory response syndrome. The effect of lipopolysaccharide (LPS), a major component of the outer surface of Gram-negative bacteria, and Staphylococcal enterotoxin B (SEB), a superantigen of Gram-positive bacteria, on cytokine production in peripheral blood mononuclear cells (PBMCs) was examined. LPS significantly increased the production of proinflammatory and anti-inflammatory cytokines, and SEB enhanced the production of helper T lymphocyte type cytokines. These results illustrated the different responses to Gram-negative and Gram-positive bacterial infections. The effect of gabexate mesilate, a synthetic protease inhibitor, on cytokine production and expression of the toll-like receptor (TLR) was also examined. The results suggest that gabexate mesilate-induced inhibition of tumour necrosis factor-alpha (TNF-alpha) and interleukin-18 (IL-18) production in LPS-stimulated PBMCs is due to the inhibition of the nuclear factor-kappa B activation pathway and/or inhibition of the processing pathway of pro-TNF-alpha and pro-IL-18, not to down-regulation of TLR-2 or TLR-4.
- Published
- 2002
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