ArticlePLoS pathogens2016
Genetic Architecture of Group A Streptococcal Necrotizing Soft Tissue Infections in the Mouse.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 33 citations in OpenAlex.
- Diagnostic strategies in necrotizing soft tissue infections: from clinical scores to multi-omics and machine learning.Burns & trauma · 2026Review
- Serial irrigation and debridement with the use of Kerecis in the treatment of necrotizing fasciitis: A case report.Trauma case reports · 2025Article
- Low expression of the CCL5 gene and low serum concentrations of CCL5 in severe invasive group a streptococcal disease.Infection · 2025Article
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Reduced interleukin-18 secretion by human monocytic cells in response to infections with hyper-virulent Streptococcus pyogenes.Journal of biomedical science · 2024Article
- Concurrent Brain Subregion Microgliosis in an HLA-II Mouse Model of Group A Streptococcal Skin Infection.Microorganisms · 2023Article
- HLA-II-Dependent Neuroimmune Changes in Group A Streptococcal Necrotizing Fasciitis.Pathogens (Basel, Switzerland) · 2023Article
- Adjunctive Rifampicin Increases Antibiotic Efficacy in Group A Streptococcal Tissue Infection Models.Antimicrobial agents and chemotherapy · 2021Article
- Article
- Metallothionein 3-Zinc Axis Suppresses Caspase-11 Inflammasome Activation and Impairs Antibacterial Immunity.Frontiers in immunology · 2021Article
- MAIT Cells Are Major Contributors to the Cytokine Response in Group A Streptococcal Toxic Shock Syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The Role of Streptococcal and Staphylococcal Exotoxins and Proteases in Human Necrotizing Soft Tissue Infections.Toxins · 2019Review
- The Collaborative Cross: A Systems Genetics Resource for Studying Host-Pathogen Interactions.Cell host & microbe · 2019Review
- The Secreted Virulence Factor NADase of Group AFrontiers in immunology · 2019Article
- Streptolysin O Induces the Ubiquitination and Degradation of Pro-IL-1β.Journal of innate immunity · 2019Article
- Heterogeneity in FoxP3- and GARP/LAP-Expressing T Regulatory Cells in an HLA Class II Transgenic Murine Model of Necrotizing Soft Tissue Infections by Group A Streptococcus.Infection and immunity · 2018Article
- Neutralization of Streptolysin S-Dependent and Independent Inflammatory Cytokine IL-1β Activity Reduces Pathology During Early Group AFrontiers in cellular and infection microbiology · 2018Article
- Article
- Association between cytokine response, the LRINEC score and outcome in patients with necrotising soft tissue infection: a multicentre, prospective study.Scientific reports · 2017Article
- Port d'Entrée for Respiratory Infections - Does the Influenza A Virus Pave the Way for Bacteria?Frontiers in microbiology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host genetic variations play an important role in several pathogenic diseases, and we have previously provided strong evidences that these genetic variations contribute significantly to differences in susceptibility and clinical outcomes of invasive Group A Streptococcus (GAS) infections, including sepsis and necrotizing soft tissue infections (NSTIs). Our initial studies with conventional mouse strains revealed that host genetic variations and sex differences play an important role in orchestrating the severity, susceptibility and outcomes of NSTIs. To understand the complex genetic architecture of NSTIs, we utilized an unbiased, forward systems genetics approach in an advanced recombinant inbred (ARI) panel of mouse strains (BXD). Through this approach, we uncovered interactions between host genetics, and other non-genetic cofactors including sex, age and body weight in determining susceptibility to NSTIs. We mapped three NSTIs-associated phenotypic traits (i.e., survival, percent weight change, and lesion size) to underlying host genetic variations by using the WebQTL tool, and identified four NSTIs-associated quantitative genetic loci (QTL) for survival on mouse chromosome (Chr) 2, for weight change on Chr 7, and for lesion size on Chr 6 and 18 respectively. These QTL harbor several polymorphic genes. Identification of multiple QTL highlighted the complexity of the host-pathogen interactions involved in NSTI pathogenesis. We then analyzed and rank-ordered host candidate genes in these QTL by using the QTLminer tool and then developed a list of 375 candidate genes on the basis of annotation data and biological relevance to NSTIs. Further differential expression analyses revealed 125 genes to be significantly differentially regulated in susceptible strains compared to their uninfected controls. Several of these genes are involved in innate immunity, inflammatory response, cell growth, development and proliferation, and apoptosis. Additional network analyses using ingenuity pathway analysis (IPA) of these 125 genes revealed interleukin-1 beta network as key network involved in modulating the differential susceptibility to GAS NSTIs.
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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.