ArticleMediators of inflammation2016
Correlation of Surface Toll-Like Receptor 9 Expression with IL-17 Production in Neutrophils during Septic Peritonitis in Mice Induced by E. coli.
Article in Mediators of inflammation, 2016. 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, 21 citations in OpenAlex.
- Pre-activation timing determines influenza severity and viral pathogenicity via STING Inhibition.Scientific reports · 2025Article
- sTLR9 on maternal Circulating immune cells as a negative regulatory phenotype during pregnancy.Cellular and molecular life sciences : CMLS · 2025Article
- B-1a cells scavenge NETs to attenuate sepsis.Journal of leukocyte biology · 2024Article
- Massively recruited sTLR9Cancer immunology, immunotherapy : CII · 2023Article
- Microcirculation and neutrophil-related cytokine concentrations are not altered around narrow diameter implants in T2DM patients during wound healing.Clinical oral investigations · 2023Article
- Surface toll-like receptor 9 on immune cells and its immunomodulatory effect.Frontiers in immunology · 2023Review
- Injection of Escherichia coli to Induce Sepsis.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Review
- Membrane TLR9 Positive Neutrophil Mediated MPLA Protects Against Fatal Bacterial Sepsis.Theranostics · 2019Article
- cfDNA correlates with endothelial damage after cardiac surgery with prolonged cardiopulmonary bypass and amplifies NETosis in an intracellular TLR9-independent manner.Scientific reports · 2017Article
- An AAAG-Rich Oligodeoxynucleotide Rescues Mice from Bacterial Septic Peritonitis by Interfering Interferon Regulatory Factor 5.International journal of molecular sciences · 2017Article
- Advanced Role of Neutrophils in Common Respiratory Diseases.Journal of immunology research · 2017Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-17 is a proinflammatory cytokine produced by various immune cells. Polymorphonuclear neutrophils (PMNs) are the first line of defense in bacterial infection and express surface Toll-like receptor 9 (sTLR9). To study the relationship of sTLR9 and IL-17 in PMNs during bacterial infection, we infected mice with E. coli intraperitoneally to establish a septic peritonitis model for studying the PMNs response in peritoneal cavity. We found that PMNs and some of "giant cells" were massively accumulated in the peritoneal cavity of mice with fatal septic peritonitis induced by E. coli. Kinetically, the CD11b(+) PMNs were increased from 20-40% at 18 hours to >80% at 72 hours after infection. After E. coli infection, sTLR9 expression on CD11b(+) and CD11b(-) PMNs and macrophages in the PLCs were increased at early stage and deceased at late stage; IL-17 expression was also increased in CD11b(+) PMNs, CD11b(-) PMNs, macrophages, and CD3(+) T cells. Using experiments of in vitro blockage, qRT-PCR and cell sorting, we confirmed that PMNs in the PLCs did increase their IL-17 expression during E. coli infection. Interestingly, sTLR9(-)CD11b(+)Ly6G(+) PMNs, not sTLR9(+)CD11b(+)Ly6G(+) PMNs, were found to be able to increase their IL-17 expression. Together, the data may help understand novel roles of PMNs in septic peritonitis.
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