ArticlePloS one2012
Neutralisation of peritoneal IL-17A markedly improves the prognosis of severe septic mice by decreasing neutrophil infiltration and proinflammatory cytokines.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Trial
- Observational
- The Emerging Roles and Therapeutic Potential of Unconventional T Cells in Sepsis.Journal of inflammation research · 2025Review
- The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy.Frontiers in microbiology · 2024Review
- Novel Aspects of the Immune Response Involved in the Peritoneal Damage in Chronic Kidney Disease Patients under Dialysis.International journal of molecular sciences · 2023Review
- Protective effect of Secukinumab on severe sepsis model rats by neutralizing IL-17A to inhibit IKBα/NFκB inflammatory signal pathway.European journal of medical research · 2022Article
- Contributory Role of BLT2 in the Production of Proinflammatory Cytokines in Cecal Ligation and Puncture-Induced Sepsis.Molecules and cells · 2021Article
- Neuroinflammation in Sepsis: Molecular Pathways of Microglia Activation.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Regulation of theInfection and immunity · 2021Article
- Article
- Identification of progranulin as a novel diagnostic biomarker for early-onset sepsis in neonates.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2020Article
- Review
- Blockade of IL-17A/IL-17R Pathway Protected Mice from Sepsis-Associated Encephalopathy by Inhibition of Microglia Activation.Mediators of inflammation · 2019Article
- IL-17, IL-27, and IL-33: A Novel Axis Linked to Immunological Dysfunction During Sepsis.Frontiers in immunology · 2019Review
- Neutralization of interleukin-17A alleviates burn-induced intestinal barrier disruption via reducing pro-inflammatory cytokines in a mouse model.Burns & trauma · 2019Article
- IL-17 in neonatal health and disease.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Review
- Interleukin-17A Aggravates Middle Ear Injury Induced by Streptococcus pneumoniae through the p38 Mitogen-Activated Protein Kinase Signaling Pathway.Infection and immunity · 2017Article
- Interleukin-17A Plays the Same Role on Mice Acute Lung Injury Respectively Induced by Lipopolysaccharide and Paraquat.Inflammation · 2017Article
- Lung-resident γδ T cells and their roles in lung diseases.Immunology · 2017Review
- Knockout of interleukin-17A protects against sepsis-associated acute kidney injury.Annals of intensive care · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe current study aimed to elucidate the role of peritoneal fluid IL-17A in septic mice, and the effects of intraperitoneal or intravenous blockade of the IL-17A pathway by anti-IL17A antibody on survival, plasma, and peritoneal cavity cytokine profile in a murine caecal ligation and puncture (CLP) sepsis model. The main source of peritoneal fluid IL-17A in septic mice was identified.
methodsMale C57BL/6 mice that underwent severe CLP or sham surgery were intraperitoneally or intravenously administered anti-IL17A antibodies or isotype antibodies. The survival rates were observed. IL-17A, TNF-α, and IL-6 cytokine levels were measured by ELISA. Surface and intracellular IL-17A immunofluorescence stains were detected by flow cytometry to identify the IL-17A-producing cells.
resultsThe IL-17A level was elevated much higher and earlier in peritoneal fluid than in the blood of the CLP mice. The intraperitoneal IL-17A blockade more significantly protects against CLP-induced mortality than intravenous blockade because of decreased TNF-α and IL-6 levels both in peritoneal fluid and blood, neutrophil infiltration in the peritoneal cavity, and lung injury. γδ T lymphocytes were identified to be the main source of IL-17A in the peritoneal fluid of septic mice.
conclusionsThe earlier and higher elevated IL-17A derived from γδ T cells in peritoneal fluid plays a critical role during polymicrobial severe sepsis and effect of intraperitoneal IL-17A antibody administration superior to intravenous administration on survival of severe CLP-induced septic mice. The intraperitoneal blockade of IL-17A decreases proinflammatory cytokine production, neutrophil infiltration, and lung injury, thereby improving septic mice survival, which provides a new potential therapy target for sepsis.
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