ArticleInflammation2021
The Anti-inflammatory Protein TSG-6 Induced by S. aureus Regulates the Chemokine Function of Endothelial Cells In Vitro by Inhibiting the Chemokine-Glycosaminoglycan Interaction.
Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- GutFrontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to explore the effect of the anti-inflammatory protein TSG-6 induced by Staphylococcus bacteria on the regulation of chemokine function in endothelial cells by inhibiting the chemokine-glycosaminoglycan interaction. To cultivate human umbilical vein endothelial cells and Staphylococcus aureus bacteria, respectively, after the experiment is divided into the control group, S. aureus bacteria-induced group, S. aureus bacteria glycosaminoglycans about 1 mg/L sugar group, S. aureus bacteria glycosaminoglycans about 5 mg/L sugar group, and S. aureus bacteria glycosaminoglycans about 10 mg/L sugar group, E-selectin; intercellular adhesion molecule-1 (ICAM-1); monocyte chemoattractant protein-1 (MCP-1); interleukin-8 (IL-8) expression level; chemokine CXCL9, CXCL10, and CXCL11 mRNA and protein expression level; and TSG mRNA and protein expression level were determined in each cell; the endothelial cell proliferation and vascular endothelial cell function indicators were analyzed. The expression levels of E-selectin, ICAM-1, IL-8, MCP-1, and chemokines CXCL9, CXCL10, and CXCL11 mRNA and protein in each group at 6, 12, and 24 h were significantly different (P < 0.05). TSG mRNA and protein expression levels, endothelial cell proliferation ability, and vascular endothelial cell function were also significantly different (P < 0.05). The expression levels of E-selectin, ICAM-1, IL-8, MCP-1, endothelial cell proliferation ability, and vascular endothelial cell function in the Staphylococcus aureus-induced group were lower than those in the control group and the Staphylococcus aureus glycosaminoglycan group, and the mRNA and protein expression levels of chemokines CXCL9, CXCL10, and CXCL11, and TSG mRNA and protein expression levels were higher. With the increase of glycosaminoglycan concentration, the above indexes were improved. The anti-inflammatory protein TSG-6 induced by S. aureus can regulate the chemokine function of endothelial cells by inhibiting the chemokine-glycosaminoglycan interaction.
Indexed as
Identifiers
What OpenQuestion holds
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.