Abstract
The combined effect of innate immunity receptors in viral-bacterial coinfections was studied in vitro using the primary culture of murine macrophages activated by different combinations of ligands of innate immunity receptors belonging to the family of Toll-like receptors. The activation of macrophages first with a viral ligand and then with a bacterial one significantly decreased the expression of proinflammatory cytokine genes. Such attenuation of immune responses may occur during the development of bacterial complications in viral infections.
MeSH terms
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Aminoquinolines / pharmacology
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Animals
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Bacterial Infections / immunology
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Bacterial Infections / metabolism
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Bone Marrow
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Cells, Cultured
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Coinfection / immunology
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Coinfection / metabolism
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Cytokines / genetics*
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Disease Models, Animal
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Imiquimod
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Immunity, Innate
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Interleukin-1beta / genetics
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Interleukin-1beta / metabolism
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Interleukin-6 / genetics
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Interleukin-6 / metabolism
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Ligands
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Lipopolysaccharides / immunology
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Macrophage Activation*
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Macrophages / immunology*
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Membrane Glycoproteins / agonists
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Membrane Glycoproteins / immunology*
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Membrane Glycoproteins / metabolism
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Mice
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Mice, Inbred C57BL
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RNA, Messenger / metabolism
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Toll-Like Receptor 4 / agonists
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Toll-Like Receptor 4 / immunology*
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Toll-Like Receptor 4 / metabolism
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Toll-Like Receptor 7 / agonists
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Toll-Like Receptor 7 / immunology*
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Toll-Like Receptor 7 / metabolism
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Toll-Like Receptors / agonists*
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Toll-Like Receptors / metabolism*
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Tumor Necrosis Factor-alpha / genetics
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Tumor Necrosis Factor-alpha / metabolism
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Virus Diseases / immunology
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Virus Diseases / metabolism
Substances
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Aminoquinolines
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Cytokines
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IL1B protein, mouse
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Interleukin-1beta
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Interleukin-6
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Ligands
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Lipopolysaccharides
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Membrane Glycoproteins
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RNA, Messenger
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Tlr4 protein, mouse
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Tlr7 protein, mouse
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Toll-Like Receptor 4
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Toll-Like Receptor 7
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Toll-Like Receptors
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Tumor Necrosis Factor-alpha
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Imiquimod