Abstract
Campylobacter jejuni is a major worldwide cause of enteric illnesses. Adult immunocompetent mice are not susceptible to C. jejuni infection. However, we show here that mice deficient in the adaptor protein myeloid differentiation factor 88 (MyD88), which is required for signaling through most Toll-like receptors, can be stably colonized by C. jejuni but not by isogenic derivatives carrying mutations in known virulence genes. We also found that Nramp1 deficiency increases the mouse susceptibility to C. jejuni infection when administered systemically. These results indicate that MyD88-deficient mice could be a useful model to study C. jejuni colonization and reveal a potential role for Nramp1 in the control of this bacterial pathogen.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Campylobacter Infections* / immunology
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Campylobacter Infections* / microbiology
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Campylobacter jejuni / genetics
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Campylobacter jejuni / immunology*
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Campylobacter jejuni / pathogenicity
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Cation Transport Proteins / deficiency
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Cation Transport Proteins / physiology*
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Colony Count, Microbial
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Cytokines / biosynthesis
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Disease Models, Animal*
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Disease Susceptibility
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Feces / microbiology
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Female
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Immunity, Innate
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Male
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Mutation
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Myeloid Differentiation Factor 88 / deficiency*
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Virulence / genetics
Substances
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Cation Transport Proteins
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Cytokines
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Myd88 protein, mouse
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Myeloid Differentiation Factor 88
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natural resistance-associated macrophage protein 1