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Cited by 189Thermal Regulation in MedicineInflammasome and immune disordersImmune Response and Inflammation

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

IL‐6 and IL‐1β in Fever: Studies Using Cytokine‐Deficient (Knockout) Mice a

KOZAK, WIESLAW, KLUGER, MATTHEW J., SOSZYNSKI, DARIUSZ, CONN, CAROLE A., RUDOLPH, KARIN, LEON, LISA R., ZHENG, HUI·1998·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.1998.tb08310.x
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Abstract

Previous data support the hypothesis that during inflammation, interleukin (IL)-1 beta and IL-6 are involved in fever, in activation of the hypothalamic-pituitary-adrenal (HPA) axis, and in the induction of eicosanoids. Most of the pathophysiologic effects of IL-1 beta and Il-6 are mediated by prostaglandins (PGs), modulated by other cytokines, and antagonized by glucocorticoids (GC), a final product of the HPA axis. To further test these relationships, we measured changes in body temperature using biotelemetry in mice deficient in genes for IL-1 beta and/or IL-6 (IL-1 beta knockout [KO] and IL-6 KO) following injection with lipopolysaccharide (LPS) to induce systemic inflammation or turpentine to induce local abscess. Circulating IL-6, tumor necrosis factor alpha (TNF-alpha), GC, and PGE2 were measured in these mice after treatment. IL-1 beta KO mice responded with reduced fever and IL-6 KO mice with normal fever to a high dose of LPS. In contrast, neither type of KO mice produced fever to turpentine. PGE2 levels (measured in the circulation) were suppressed in both types of KO mice injected with turpentine. IL-1 beta KO mice showed deficiency in IL-6 following turpentine, but not LPS, injection. LPS-induced increases in TNF-alpha did not differ between IL-1 beta KO mice and their wild-type counterparts, whereas IL-6 KO mice showed exacerbated LPS-induced circulating TNF-alpha. No differences were noted in plasma elevations of GC between KO and wild-type mice following injection of LPS or turpentine, indicating that IL-1 beta and IL-6 are not required for activation of the HPA axis during inflammation. Our data demonstrate that in the mouse, IL-1 beta and IL-6 are critical for the induction of fever during local inflammation, whereas in systemic inflammation they appear only to contribute to fever.

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Crossref · 10.1111/j.1749-6632.1998.tb08310.x

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Citations

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Research works printed but not linked: 9

  1. Blatteis C. M., 1997, Fever: How may circulating pyrogens signal the brain? News Physiol, Sci., 12, 1
  2. Kozak W., 1995, Thermal and behavioral effects of lipopolysaccharide and influenza in interleukin‐1β‐deficient mice, Am. J. Physiol., 269, R969
  3. Rothwell N. J. N. J. Busbridge H. Humphrey & P. Hissey. 1990. Central actions of interleukin‐1β on fever and thermogenesis.InThe Physiological and Pathological Effects of Cytokines. C. A. Dinarello M. J. Kluger M. C. Powanda & J. J. Oppenheim Eds.: 307‐311. Wiley‐Liss. New York.
  4. Long N. C., 1990, The roles of interleukin‐1β and tumor necrosis factor in lipopolysaccharide fever in the rat, Am. J. Physiol., 259, R724
  5. Klir J. J., 1994, Interleukin‐1β causes the increase in anterior hypothalamic interleukin‐6 during LPS‐induced fever in rats, Am. J. Physiol., 266, R1845
  6. Smith B. K., 1992, Human IL‐1 receptor antagonist partially suppresses LPS fever but not plasma levels of IL‐6 in the Fisher rat, Am. J. Physiol., 263, R653
  7. Leon L. R., 1995, Attenuation of central interleukin‐1β fever following type I but not type II receptor antagonism in rats, FASEB J., 9, A645
  8. Cooper A. L., 1994, Tumor necrosis factor‐α and fever after peripheral inflammation in the rat, Am. J. Physiol., 267, R1431
  9. 10.1210/en.132.3.946 · DOI

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Metadata

Authors
KOZAK, W., KLUGER, M. J., SOSZYNSKI, D., CONN, C. A., RUDOLPH, K., LEON, L. R., & ZHENG, H.
Affiliations
  • Lovelace Respiratory Research Institute (US)
  • Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
ORCID
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
1998-09
Volume
856
Issue
1
Pages
33-47
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.1998.tb08310.x
OpenAlex
W2042477580
Cited by
189
References
31
Citations by year
2026: 4 · 2025: 2 · 2024: 8 · 2023: 6 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 9 · 2018: 8 · 2017: 7 · 2016: 6 · 2015: 6 · 2014: 5 · 2013: 7 · 2012: 3
FWCI
5.83
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 2716 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (2r01ai027556-06a1)
  • National Institute of Allergy and Infectious Diseases (AI27556)
Topics
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Thermal Regulation in Medicine
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
fever, IL-1β, interleukin-6, cytokine knockout mice, lipopolysaccharide, prostaglandin E2, TNF-α, glucocorticoids, hypothalamic-pituitary-adrenal axis, systemic inflammation, local inflammation, body temperature
MeSH terms
Animals, Chimera, Escherichia coli, Female, Fever, Inflammation, Interleukin-1, Lipopolysaccharides, Male, Time Factors, Tumor Necrosis Factor-alpha, Turpentine, Dinoprostone, Interleukin-6, Mice, Knockout, Mice

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