ArticlePLoS pathogens2008
An unbiased systems genetics approach to mapping genetic loci modulating susceptibility to severe streptococcal sepsis.
Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Genetic Architecture of Group A Streptococcal Necrotizing Soft Tissue Infections in the Mouse.PLoS pathogens · 2016Article
- Host Genetic Variations and Sex Differences Potentiate Predisposition, Severity, and Outcomes of Group A Streptococcus-Mediated Necrotizing Soft Tissue Infections.Infection and immunity · 2016Article
- Mapping of genetic loci that modulate differential colonization by Escherichia coli O157:H7 TUV86-2 in advanced recombinant inbred BXD mice.BMC genomics · 2015Article
- Inflammasome/IL-1β Responses to Streptococcal Pathogens.Frontiers in immunology · 2015Review
- Host responses to group a streptococcus: cell death and inflammation.PLoS pathogens · 2014Review
- Genetic control of weight loss during pneumonic Burkholderia pseudomallei infection.Pathogens and disease · 2014Article
- Effects of selective and nonselective nonsteroidal anti-inflammatory drugs on antibiotic efficacy of experimental group A streptococcal myonecrosis.The Journal of infectious diseases · 2014Article
- Genetic variation in Chlamydia trachomatis and their hosts: impact on disease severity and tissue tropism.Future microbiology · 2013Review
- Intrauterine group A streptococcal infections are exacerbated by prostaglandin E2.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Article
- Development of a murine model for aerosolized ebolavirus infection using a panel of recombinant inbred mice.Viruses · 2012Review
- E-prostanoid 2 receptor signaling suppresses lung innate immunity against Streptococcus pneumoniae.Prostaglandins & other lipid mediators · 2012Article
- Interferon-γ-producing immature myeloid cells confer protection against severe invasive group A Streptococcus infections.Nature communications · 2012Article
- Postpartum group a Streptococcus sepsis and maternal immunology.American journal of reproductive immunology (New York, N.Y. : 1989) · 2012Review
- Host genetics and Chlamydia disease: prediction and validation of disease severity mechanisms.PloS one · 2012Article
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- Article
- The stanley neuropathology consortium integrative database: a novel, web-based tool for exploring neuropathological markers in psychiatric disorders and the biological processes associated with abnormalities of those markers.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010Article
- A decade of molecular pathogenomic analysis of group A Streptococcus.The Journal of clinical investigation · 2009Review
- Population biology of the human restricted pathogen, Streptococcus pyogenes.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Striking individual differences in severity of group A streptococcal (GAS) sepsis have been noted, even among patients infected with the same bacterial strain. We had provided evidence that HLA class II allelic variation contributes significantly to differences in systemic disease severity by modulating host responses to streptococcal superantigens. Inasmuch as the bacteria produce additional virulence factors that participate in the pathogenesis of this complex disease, we sought to identify additional gene networks modulating GAS sepsis. Accordingly, we applied a systems genetics approach using a panel of advanced recombinant inbred mice. By analyzing disease phenotypes in the context of mice genotypes we identified a highly significant quantitative trait locus (QTL) on Chromosome 2 between 22 and 34 Mb that strongly predicts disease severity, accounting for 25%-30% of variance. This QTL harbors several polymorphic genes known to regulate immune responses to bacterial infections. We evaluated candidate genes within this QTL using multiple parameters that included linkage, gene ontology, variation in gene expression, cocitation networks, and biological relevance, and identified interleukin1 alpha and prostaglandin E synthases pathways as key networks involved in modulating GAS sepsis severity. The association of GAS sepsis with multiple pathways underscores the complexity of traits modulating GAS sepsis and provides a powerful approach for analyzing interactive traits affecting outcomes of other infectious diseases.
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Registered trials
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.