Cited by 300Immune Response and InflammationSepsis Diagnosis and TreatmentInflammation biomarkers and pathways

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Evidence for IFN-gamma as a mediator of the lethality of endotoxin and tumor necrosis factor-alpha

Doherty, G M, Lange, J R, Langstein, H N, Alexander, H R, Buresh, C M, Norton, J A·1992·The Journal of Immunology

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Abstract

Current evidence indicates that endogenously produced peptide cytokines, most notably TNF-alpha and IL-1, mediate the lethality of experimental endotoxemia. Because circulating serum levels of IFN-gamma can be detected soon after TNF-alpha and IL-1 in response to endotoxin, we investigated the role of IFN-gamma in endotoxin and TNF-alpha lethality. Specific neutralizing antibodies to murine TNF-alpha (anti-TNF-alpha Ab) or murine IFN gamma (anti-IFN-gamma Ab) produced in our laboratory protected mice against the lethality of Escherichia coli endotoxin (LPS) administered 6 h later. Serum IFN-gamma levels 2 h after i.v. LPS were lower in mice treated with anti-TNF-alpha Ab compared to mice that received nonimmune IgG (median less than 2.5 vs 3.0 U/ml, P2 less than 0.05). In contrast, serum TNF-alpha levels 1 h after i.v. LPS peaked more than fourfold higher in mice treated with anti-IFN-gamma Ab compared to controls (median greater than 6400 vs 1405 pg/ml, p2 less than 0.05). Doses of TNF-alpha (300 micrograms/kg) and IFN-gamma (50,000 U) which were well tolerated when given individually were synergistically lethal in combination (0% lethality vs 100% lethality, P2 less than 0.001), and were associated with higher serum levels of IL-6 than with either cytokine alone. Anti-IFN-gamma Ab provided complete protection against exogenous human rTNF-alpha at the LD100 dose (1400 micrograms/kg, p2 less than 0.001), and in fact prevented lethality at doses four- to fivefold greater than the LD100 human rTNF-alpha (up to 6000 micrograms/kg). We conclude that IFN-gamma is synergistic with TNF-alpha, is essential for the lethality of LPS and TNF-alpha, and may have modulating effects on the negative control of serum levels of TNF-alpha after LPS in mice.

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Authors: Doherty, G. M., Lange, J. R., Langstein, H. N., Alexander, H. R., Buresh, C. M., & Norton, J. A.
Affiliations: National Institutes of Health (US)
ORCID: Doherty, G M
Langstein, H N
Norton, J A
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 1992-09-01
Volume: 149
Issue: 5
Pages: 1666-1670
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.149.5.1666
OpenAlex: W1946578458
Cited by: 300
References: 0
Citations by year: 2026: 1 · 2025: 3 · 2024: 4 · 2023: 1 · 2022: 7 · 2021: 6 · 2020: 6 · 2019: 3 · 2018: 4 · 2016: 2 · 2015: 5 · 2014: 4 · 2013: 5 · 2012: 6
FWCI: 7.41
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Sepsis Diagnosis and Treatment
Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords: interferon-gamma, TNF-α, endotoxemia, cytokine synergy, anti-TNF-alpha antibody, anti-IFN-gamma antibody, interleukin-6, serum cytokine levels, endotoxin tolerance, sepsis
MeSH terms: Animals, Antibodies, Endotoxins, Female, Interferon-gamma, Lipopolysaccharides, Mice, Inbred C3H, Rabbits, Tumor Necrosis Factor-alpha, Interleukin-6, Mice

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Evidence for IFN-gamma as a mediator of the lethality of endotoxin and tumor necrosis factor-alpha

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