Abstract
Septic syndrome is a consequence of innate immune failure. Recent studies showed that the CC chemokine CCL6 enhanced antimicrobial immunity during experimental sepsis through an unknown mechanism. The present study demonstrates that transgenic CCL6 expression abolishes mortality in a septic peritonitis model via the modulation of resident peritoneal cell activation and, more importantly, through the recruitment of IFN-producing NK cells and killer dendritic cells into the peritoneum. Thus, CCL6 attenuates the immune failure during sepsis, in part, through a protective type 1-cytokine mediated mechanism.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Cell Movement / immunology*
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Cells, Cultured
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Chemokines, CC / biosynthesis
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Chemokines, CC / genetics
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Chemokines, CC / physiology*
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Dendritic Cells / cytology
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Dendritic Cells / immunology
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Dendritic Cells / metabolism
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Female
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Immunity, Innate*
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Interferon-gamma / biosynthesis
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Interferon-gamma / physiology
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Killer Cells, Natural / cytology
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Killer Cells, Natural / immunology
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Killer Cells, Natural / metabolism
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Macrophage Activation / immunology
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Macrophages, Peritoneal / cytology
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Macrophages, Peritoneal / immunology
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Macrophages, Peritoneal / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Peritoneum / cytology*
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Peritoneum / immunology*
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Peritoneum / metabolism
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Peritonitis / immunology
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Peritonitis / metabolism
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Peritonitis / pathology
Substances
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Chemokines, CC
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Ccl6 protein, mouse
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Interferon-gamma