Role of Salmonella typhimurium mn-superoxide dismutase (SodA) in protection against early killing by J774 macrophages

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Abstract

The Salmonella typhimurium gene for Mn-cofactored superoxide dismutase (sodA) was cloned by complementation of an Escherichia coli soda sodB mutant for growth on minimal medium. Sequence analysis revealed an open reading frame of 618 bp encoding a polypeptide with 97% identity to E. coli SodA. A S. typhimurium soda mutant was created by allelic exchange and tested for the ability to survive in the murine macrophage-like cell line J774. Growth of bacteria under iron-limiting conditions, inactivation of the Fur repressor, or expression of sodA from a plasmid resulted in increased resistance to early killing by J774 cells, which was abolished in the soda mutant. These results suggest that resistance to the early oxygen-dependent microbicidal mechanisms of phagocytes involves the SodA gene product. The S. typhimurium sodA mutant was not significantly attenuated in mice, however, which suggests that resistance to early oxygen-dependent microbicidal mechanisms in vivo may play only a minor role in Salmonella pathogenesis.

Original languageEnglish (US)
Pages (from-to)1739-1744
Number of pages6
JournalInfection and Immunity
Volume63
Issue number5
StatePublished - 1995
Externally publishedYes

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Salmonella typhimurium
Superoxide Dismutase
Macrophages
Oxygen
Escherichia coli
Phagocytes
Growth
Salmonella
Open Reading Frames
Genes
Sequence Analysis
Plasmids
Iron
Bacteria
Cell Line
Peptides

ASJC Scopus subject areas

  • Immunology

Cite this

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title = "Role of Salmonella typhimurium mn-superoxide dismutase (SodA) in protection against early killing by J774 macrophages",
abstract = "The Salmonella typhimurium gene for Mn-cofactored superoxide dismutase (sodA) was cloned by complementation of an Escherichia coli soda sodB mutant for growth on minimal medium. Sequence analysis revealed an open reading frame of 618 bp encoding a polypeptide with 97{\%} identity to E. coli SodA. A S. typhimurium soda mutant was created by allelic exchange and tested for the ability to survive in the murine macrophage-like cell line J774. Growth of bacteria under iron-limiting conditions, inactivation of the Fur repressor, or expression of sodA from a plasmid resulted in increased resistance to early killing by J774 cells, which was abolished in the soda mutant. These results suggest that resistance to the early oxygen-dependent microbicidal mechanisms of phagocytes involves the SodA gene product. The S. typhimurium sodA mutant was not significantly attenuated in mice, however, which suggests that resistance to early oxygen-dependent microbicidal mechanisms in vivo may play only a minor role in Salmonella pathogenesis.",
author = "Tsolis, {Renee M} and Baumler, {Andreas J} and F. Heffron",
year = "1995",
language = "English (US)",
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issn = "0019-9567",
publisher = "American Society for Microbiology",
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T1 - Role of Salmonella typhimurium mn-superoxide dismutase (SodA) in protection against early killing by J774 macrophages

AU - Tsolis, Renee M

AU - Baumler, Andreas J

AU - Heffron, F.

PY - 1995

Y1 - 1995

N2 - The Salmonella typhimurium gene for Mn-cofactored superoxide dismutase (sodA) was cloned by complementation of an Escherichia coli soda sodB mutant for growth on minimal medium. Sequence analysis revealed an open reading frame of 618 bp encoding a polypeptide with 97% identity to E. coli SodA. A S. typhimurium soda mutant was created by allelic exchange and tested for the ability to survive in the murine macrophage-like cell line J774. Growth of bacteria under iron-limiting conditions, inactivation of the Fur repressor, or expression of sodA from a plasmid resulted in increased resistance to early killing by J774 cells, which was abolished in the soda mutant. These results suggest that resistance to the early oxygen-dependent microbicidal mechanisms of phagocytes involves the SodA gene product. The S. typhimurium sodA mutant was not significantly attenuated in mice, however, which suggests that resistance to early oxygen-dependent microbicidal mechanisms in vivo may play only a minor role in Salmonella pathogenesis.

AB - The Salmonella typhimurium gene for Mn-cofactored superoxide dismutase (sodA) was cloned by complementation of an Escherichia coli soda sodB mutant for growth on minimal medium. Sequence analysis revealed an open reading frame of 618 bp encoding a polypeptide with 97% identity to E. coli SodA. A S. typhimurium soda mutant was created by allelic exchange and tested for the ability to survive in the murine macrophage-like cell line J774. Growth of bacteria under iron-limiting conditions, inactivation of the Fur repressor, or expression of sodA from a plasmid resulted in increased resistance to early killing by J774 cells, which was abolished in the soda mutant. These results suggest that resistance to the early oxygen-dependent microbicidal mechanisms of phagocytes involves the SodA gene product. The S. typhimurium sodA mutant was not significantly attenuated in mice, however, which suggests that resistance to early oxygen-dependent microbicidal mechanisms in vivo may play only a minor role in Salmonella pathogenesis.

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