Abstract
Salmonella species cause substantial morbidity, mortality and burden of disease globally. Infections with Salmonella species cause multiple clinical syndromes. Central to the pathophysiology of all human salmonelloses is the induction of a strong host innate immune/inflammatory response. Whether this ultimately reflects an adaptive advantage to the host or pathogen is not clear. However, it is evident that both the host and pathogen have evolved mechanisms of triggering host responses that are detrimental to the other. In this review, we explore some of the host and pathogenic mechanisms mobilized in the two predominant clinical syndromes associated with infection with Salmonella enterica species: enterocolitis and typhoid.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Bacterial Proteins / genetics
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Bacterial Proteins / physiology
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Cytokines / physiology
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Diarrhea / etiology
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Diarrhea / microbiology
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Disease Susceptibility / immunology
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Enterocolitis / etiology
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Enterocolitis / immunology*
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Enterocolitis / microbiology*
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Host-Parasite Interactions*
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Humans
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Immunity, Innate / physiology
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Inflammation / etiology
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NF-kappa B / physiology
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Neutrophil Infiltration / physiology
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Salmonella / genetics
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Salmonella / pathogenicity*
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Salmonella Infections / immunology*
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Salmonella Infections / microbiology
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Toll-Like Receptor 4 / physiology
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Virulence Factors / immunology
Substances
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Bacterial Proteins
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Cytokines
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NF-kappa B
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Tlr4 protein, mouse
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Toll-Like Receptor 4
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Virulence Factors