ArticleInfection and immunity2009
CD46 transgenic mouse model of necrotizing fasciitis caused by Streptococcus pyogenes infection.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Advances in Necrotizing Fasciitis Animal Models: Current Trends and Future Perspectives.Journal of inflammation research · 2025Review
- Mechanisms of host adaptation by bacterial pathogens.FEMS microbiology reviews · 2024Review
- The Role of Gram-Positive Surface Proteins in Bacterial Niche- and Host-Specialization.Frontiers in microbiology · 2020Review
- Inflammatory Joint Disease Is a Risk Factor for Streptococcal Sepsis and Septic Arthritis in Mice.Frontiers in immunology · 2020Article
- Towards developing a vaccine for rheumatic heart disease.Global cardiology science & practice · 2017Review
- Genetic Dissection of the Host Tropism of Human-Tropic Pathogens.Annual review of genetics · 2015Review
- Functional genomic characterization of virulence factors from necrotizing fasciitis-causing strains of Aeromonas hydrophila.Applied and environmental microbiology · 2014Article
- Bacterial superantigens promote acute nasopharyngeal infection by Streptococcus pyogenes in a human MHC Class II-dependent manner.PLoS pathogens · 2014Article
- Molecular basis of host specificity in human pathogenic bacteria.Emerging microbes & infections · 2014Review
- Lactobacilli reduce cell cytotoxicity caused by Streptococcus pyogenes by producing lactic acid that degrades the toxic component lipoteichoic acid.Antimicrobial agents and chemotherapy · 2011Article
- [Necrotizing fasciitis. 2011 update].Der Unfallchirurg · 2011Article
- Tissue tropisms in group A streptococcal infections.Future microbiology · 2010Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We developed a human CD46-expressing transgenic (Tg) mouse model of subcutaneous (s.c.) infection into both hind footpads with clinically isolated 11 group A streptococcus (GAS) serotype M1 strains. When the severity levels of foot lesions at 72 h and the mortality rates by 336 h were compared after s.c. infection with 1x10(7) CFU of each GAS strain, the GAS472 strain, isolated from the blood of a patient suffering from streptococcal toxic shock syndrome (STSS), induced the highest severity levels and mortality rates. GAS472 led to a 100% mortality rate in CD46 Tg mice after only 168 h postinfection through the supervention of severe necrotizing fasciitis (NF) of the feet. In contrast, GAS472 led to a 10% mortality rate in non-Tg mice through the supervention of partial necrotizing cutaneous lesions of the feet. The footpad skin sections of CD46 Tg mice showed hemorrhaging and necrotic striated muscle layers in the dermis, along with the exfoliation of epidermis with intracellular edema until 48 h after s.c. infection with GAS472. Thereafter, the bacteria proliferated, reaching a 90-fold or 7-fold increase in the livers of CD46 Tg mice or non-Tg mice, respectively, for 24 h between 48 and 72 h after s.c. infection with GAS472. As a result, the infected CD46 Tg mice appeared to suffer severe liver injuries. These findings suggest that human CD46 enhanced the progression of NF in the feet and the exponential growth of bacteria in deep tissues, leading to death.
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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.