ArticleJournal of biomedical science2016
Syndecan-1 (CD138) deficiency increases Staphylococcus aureus infection but has no effect on pathology in a mouse model of peritoneal dialysis.
Article in Journal of biomedical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 3 citations in OpenAlex.
- Elevated Serum and Cerebrospinal Fluid CD138 in Patients With Anti-Frontiers in molecular neuroscience · 2019Article
- Role and Molecular Mechanisms of Pericytes in Regulation of Leukocyte Diapedesis in Inflamed Tissues.Mediators of inflammation · 2019Review
- Antimicrobial Efficacy of a New Chlorhexidine-based Device Against Staphylococcus aureus Colonization of Venous Catheters.Journal of infusion nursing : the official publication of the Infusion Nurses SocietyArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTechnique failure in peritoneal dialysis (PD) due to fibrosis and angiogenesis is complicated by peritonitis. Staphylococcus aureus infection is one of the most common causes of peritonitis in PD. The heparan sulfate proteoglycan, syndecan-1 (CD138), was reported to regulate fibrosis, angiogenesis, inflammation and S. aureus infection. The objectives of this study were to examine the effects of syndecan-1 on S. aureus infection and histopathology in a PD model.
resultsSyndecan-1(-/-) and wild type mice were dialyzed for 4 weeks and infected intraperitoneally with S. aureus. Tissues were collected after 4 h for histomorphometric analysis. Intravital microscopy was used to observe leukocyte recruitment and to quantify syndecan-1 in the parietal peritoneum microcirculation. The dialyzed syndecan-1(-/-) mice were more susceptible to S. aureus infection than undialyzed syndecan-1(-/-) controls and wild type animals. However, peritoneal fibrosis and neovascularization due to PD did not differ between syndecan-1(-/-) and wild type mice. Intravital microscopy showed that in S. aureus infection, syndecan-1 was removed from the subendothelial layer of peritoneal venules but syndecan-1 deficiency did not affect leukocyte recruitment.
conclusionsThis study indicates that, while syndecan-1 is important for providing a barrier to acute S. aureus infection in PD, it does not affect peritoneal fibrosis and angiogenesis.
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