ArticleInfection and immunity2001
Contribution of Mn-cofactored superoxide dismutase (SodA) to the virulence of Streptococcus agalactiae.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
77 citing papers in PubMed, 156 citations in OpenAlex.
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- The impact of nutritional immunity on Group B streptococcal pathogenesis during wound infection.mBio · 2023Article
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- Streptococcal peptides and their roles in host-microbe interactions.Frontiers in cellular and infection microbiology · 2023Review
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- The Role of Regulator Catabolite Control Protein A (CcpA) in Streptococcus agalactiae Physiology and Stress Response.Microbiology spectrum · 2022Article
- Streptococcus agalactiaemBio · 2022Article
- Streptococcus agalactiae cadD alleviates metal stress and promotes intracellular survival in macrophages and ascending infection during pregnancy.Nature communications · 2022Article
- Population genomics of Group B Streptococcus reveals the genetics of neonatal disease onset and meningeal invasion.Nature communications · 2022Article
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- PerR-Regulated Manganese Import Contributes to Oxidative Stress Defense in Streptococcus suis.Applied and environmental microbiology · 2022Article
- The impact of Lactobacillus on group B streptococcal interactions with cells of the extraplacental membranes.Microbial pathogenesis · 2020Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Superoxide dismutases convert superoxide anions to molecular oxygen and hydrogen peroxide, which, in turn, is metabolized by catalases and/or peroxidases. These enzymes constitute one of the major defense mechanisms of cells against oxidative stress and hence play a role in the pathogenesis of certain bacteria. We previously demonstrated that group B streptococci (GBS) possess a single Mn-cofactored superoxide dismutase (SodA). To analyze the role of this enzyme in the pathogenicity of GBS, we constructed a sodA-disrupted mutant of Streptococcus agalactiae NEM316 by allelic exchange. This mutant was subsequently cis complemented by integration into the chromosome of pAT113/Sp harboring the wild-type sodA gene. The SOD specific activity detected by gel analysis in cell extracts confirmed that active SODs were present in the parental and complemented strains but absent in the sodA mutant. The growth rates of these strains in standing cultures were comparable, but the sodA mutant was extremely susceptible to the oxidative stress generated by addition of paraquat or hydrogen peroxide to the culture medium and exhibited a higher mutation frequency in the presence of rifampin. In mouse bone marrow-derived macrophages, the sodA mutant showed an increased susceptibility to bacterial killing by macrophages. In a mouse infection model, after intravenous injection the survival of the sodA mutant in the blood and the brain was markedly reduced in comparison to that of the parental and complemented strains whereas only minor effects on survival in the liver and the spleen were observed. These results suggest that SodA plays a role in GBS pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.