ArticleInfection and immunity1996
Role of the staphylococcal accessory gene regulator (sar) in septic arthritis.
Article in Infection and immunity, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 54 citations in OpenAlex.
- Utilization of In Vivo Imaging System to Study Staphylococcal Sepsis and Septic Arthritis Progression in Mouse Model.Pathogens (Basel, Switzerland) · 2024Article
- Exploring the role of bacterial virulence factors and host elements in septic arthritis: insights from animal models for innovative therapies.Frontiers in microbiology · 2024Review
- Celastrol mitigates staphyloxanthin biosynthesis and biofilm formation in Staphylococcus aureus via targeting key regulators of virulence; in vitro and in vivo approach.BMC microbiology · 2022Article
- Article
- RpiRc Is a Pleiotropic Effector of Virulence Determinant Synthesis and Attenuates Pathogenicity in Staphylococcus aureus.Infection and immunity · 2016Article
- Sigma Factor SigB Is Crucial to Mediate Staphylococcus aureus Adaptation during Chronic Infections.PLoS pathogens · 2015Article
- Attenuating Staphylococcus aureus virulence gene regulation: a medicinal chemistry perspective.Journal of medicinal chemistry · 2013Article
- sarA-mediated repression of protease production plays a key role in the pathogenesis of Staphylococcus aureus USA300 isolates.Molecular microbiology · 2012Article
- Evaluation of capsular and acapsular strains of S. aureus in an experimental brain abscess model.Journal of neuroimmunology · 2010Article
- mgrA regulates staphylococcal virulence important for induction and progression of septic arthritis and sepsis.Microbes and infection · 2008Article
- Induction of multiple matrix metalloproteinases in human dermal and synovial fibroblasts by Staphylococcus aureus: implications in the pathogenesis of septic arthritis and other soft tissue infections.Arthritis research & therapy · 2006Article
- Sigma factor B and RsbU are required for virulence in Staphylococcus aureus-induced arthritis and sepsis.Infection and immunity · 2004Article
- Caenorhabditis elegans as a model host for Staphylococcus aureus pathogenesis.Infection and immunity · 2003Article
- Role of sarA in the pathogenesis of Staphylococcus aureus musculoskeletal infection.Infection and immunity · 2003Article
- Strain-dependent differences in the regulatory roles of sarA and agr in Staphylococcus aureus.Infection and immunity · 2002Article
- Diminished virulence of an alpha-toxin mutant of Staphylococcus aureus in experimental brain abscesses.Infection and immunity · 2001Article
- Variance in fibronectin binding and fnb locus polymorphisms in Staphylococcus aureus: identification of antigenic variation in a fibronectin binding protein adhesin of the epidemic CMRSA-1 strain of methicillin-resistant S. aureus.Infection and immunity · 2001Article
- Study of Staphylococcus aureus pathogenic genes by transfer and expression in the less virulent organism Streptococcus gordonii.Infection and immunity · 2001Article
- Functional analysis of the Staphylococcus aureus collagen adhesin B domain.Infection and immunity · 1999Article
- Factors affecting the collagen binding capacity of Staphylococcus aureus.Infection and immunity · 1998Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus aureus arthritis is a highly erosive disease in which both host and bacterial factors are of importance for its induction and progression. At the transcriptional level, three known loci act in regulating production of exoproteins and expression of cell wall structures. The aim of our study was to assess the role of the sar locus as a virulence determinant in the pathogenesis of septic arthritis. A recently established murine model of hematogenously spread S. aureus arthritis was employed. S. aureus strains, isogenic for the sar locus, were inoculated intravenously into NMRI mice, and the clinical, bacteriological, serological, and histopathological progression of the disease was studied. Within 1 week after inoculation of bacteria, the frequency of arthritis was 79% in the group of mice inoculated with the sar+ strain, whereas the corresponding frequency in sar mutants was 21% (P < 0.01). Mice inoculated with the sar+ staphylococcal strain exhibited a more pronounced T- and B-lymphocyte activation than those inoculated with the sar mutant, evidenced by splenomegaly, polyclonal B-cell activation, and high serum levels of interleukin 6 and gamma interferon. Also, infection with sar+ staphylococci induced a pronounced weight loss. To assess the relationship between clinical signs and spread of bacteria, we analyzed the homing pattern and persistence of S. aureus in host tissues. Kidneys and joints from sar+-inoculated subjects displayed a higher degree of bacterial persistence than other organs. Our results suggest that molecules controlled by the sar locus are important virulence determinants in the induction and progression of septic arthritis.
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