ArticleClinical and diagnostic laboratory immunology1997
Endotoxin-induced lethality in neonatal mice is counteracted by interleukin-10 (IL-10) and exacerbated by anti-IL-10.
Article in Clinical and diagnostic laboratory immunology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Soluble epoxide hydrolase inhibition reverses cognitive dysfunction in a mouse model of metabolic syndrome by modulating inflammation.Prostaglandins & other lipid mediators · 2024Article
- IL-10 Has Differential Effects on the Innate and Adaptive Immune Systems of Septic Patients.Journal of immunology (Baltimore, Md. : 1950) · 2019Observational
- Cardiac function and circulating cytokines after endotoxin exposure in neonatal mice.Pediatric research · 2010Article
- Hypoxia-inducible factor 2alpha regulates macrophage function in mouse models of acute and tumor inflammation.The Journal of clinical investigation · 2010Article
- Hypoxia-inducible factors as essential regulators of inflammation.Current topics in microbiology and immunology · 2010Review
- The interaction of oxidative stress response with cytokines in the thyrotoxic rat: is there a link?Mediators of inflammation · 2009Article
- Prevention and treatment of lethal murine endotoxemia by the novel immunomodulatory agent MFP-14.Antimicrobial agents and chemotherapy · 2001Article
- Mechanism of T-cell mediated protection in newborn mice against a Chlamydia infection.Microbes and infectionArticle
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lethal effects occurring in neonatal (<24-h-old) BALB/c mice after challenge with 25 mg of lipopolysaccharide (LPS) per kg of body weight were significantly counteracted by pretreatment with recombinant interleukin-10 (rIL-10; 25 or 50 ng/mouse). Concordantly, blockage of endogenous IL-10 with the SXC1 monoclonal antibody increased LPS-induced mortality. Both IL-10 and SXC1 modulated the release of tumor necrosis factor alpha (TNF-alpha) so that, relative to controls, peak TNF-alpha values after LPS challenge were decreased by rIL-10 and increased by anti-IL-10.
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Registered trials
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