ArticleBritish journal of pharmacology2006
Systemic administration of interleukin-2 inhibits inflammatory neutrophil migration: role of nitric oxide.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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
7 citing papers in PubMed, 23 citations in OpenAlex.
- Predictors of bacterial pneumonia in Evaluation of Subcutaneous Interleukin-2 in a Randomized International Trial (ESPRIT).HIV medicine · 2011Trial
- Tumor-Infiltrating Lymphocyte Cell Therapy for the Treatment of Advanced Melanoma: From Patient Identification to Posttreatment Management.Journal of the advanced practitioner in oncology · 2025Review
- CU06-1004 as a promising strategy to improve anti-cancer drug efficacy by preventing vascular leaky syndrome.Frontiers in pharmacology · 2023Article
- Neutrophil extracellular traps (NETs) exacerbate severity of infant sepsis.Critical care (London, England) · 2019Article
- Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis.Arthritis research & therapy · 2017Article
- Apocynin and Nox2 regulate NF-κB by modifying thioredoxin-1 redox-state.Scientific reports · 2016Article
- Pivotal role of the 5-lipoxygenase pathway in lung injury after experimental sepsis.American journal of respiratory cell and molecular biology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Interleukin-2 (IL-2) has proinflammatory properties that limit its therapeutic use. Its side effects are mainly explained by the induction of a vascular leakage syndrome. Cytokines, as TNF-alpha and IL-1beta, and nitric oxide (NO) generated by IL-2-activated leukocytes play a role in this defect. 2. As the systemic release of these mediators inhibits neutrophil migration to a specific inflammatory site, we investigated now whether IL-2 administrated systemically inhibits the neutrophil recruitment to the inflamed peritoneum. The involvement of NO in the process was also addressed. 3. Using peritoneal neutrophils, we show that the intravenous treatment of the mice with IL-2 inhibits the neutrophil migration induced by carrageenin, LPS or fMLP. In confirmation, IL-2-treated mice showed a significant reduction in leukocyte rolling and adhesion in mesenteric microcirculation evaluated after carrageenin, LPS and fMLP injections. Aminoguanidine prevented the inhibitory effect of IL-2 on carrageenin-induced neutrophil migration, rolling and adhesion. In contrast, IL-2 failed to reduce the lung leukocyte infiltration induced by LPS. Therefore, IL-2 inhibition of neutrophil migration is organ specific. 4. Our results indicate that IL-2 administered systemically inhibits neutrophil recruitment to some inflammatory sites through a mechanism dependent on NO. The results also reinforce the needs to determine the mechanism by which patients treated with IL-2 show increased risks of infection.
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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.