The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
Circulating Cytokines as Mediators of Fever
Abstract
The febrile response is thought to be mediated by endogenous mediators, generically called "endogenous pyrogens." In the classical model of pathogenesis, induction of fever is mediated by the release of pyrogenic cytokines such as tumor necrosis factor (TNF), interleukin (IL)-1, IL-6, and interferons into the bloodstream in response to exogenous pyrogens. These mediators act at the level of the organum vasculosum of the lamina terminalis in the central nervous system (CNS), inducing synthesis of prostaglandins, which are the central mediators of the coordinated responses leading to fever. However, analysis of recent data suggests that multiple pathways may be involved in the induction of fever by cytokines, such as local cytokine production leading to signaling through vagal fibers, release of cytokine-induced circulating mediators at the tissue level, the use of membrane-bound cytokines as mediators, or the local release of cytokines in the hypothalamus by circulating activated monocytes. In addition, certain bacterial products can stimulate cytokine production directly at the level of hypothalamus, probably by activation of Toll-like receptors. A multipathway mechanism for the induction of fever is therefore suggested.
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Cites
Receptor-Dependent Mechanisms of Cell Stimulation by Bacterial Endotoxin
Ulevitch, R. J., & Tobias, P. S. (1995) · Annual Review of Immunology · doi:10.1146/annurev.iy.13.040195.002253 · Cited by 1,442 · cited 1×
“An additional important factor for the ligand-receptor interaction is a plasma factor, LPS-binding protein, which transfers LPS from the circulating micellae to the receptor complex [74].”
BackgroundImpaired febrile response in mice lacking the prostaglandin E receptor subtype EP3
Ushikubi, F., Segi, E., Sugimoto, Y., Murata, T., Matsuoka, T., Kobayashi, T., Hizaki, H., Tuboi, K., Katsuyama, M., Ichikawa, A., et al. (1998) · Nature · doi:10.1038/26233 · Cited by 677 · cited 1×
“A long-standing debate regarding the need for PG in the induction of fever, or of other mediators such as corticotrophinreleasing factor or platelet-activating factor [6], has been recently settled by showing that mice lacking the PGE receptor subtype EP3 are not able to develop a febrile response [21].”
BackgroundHorai, R., Asano, M., Sudo, K., Kanuka, H., Suzuki, M., Nishihara, M., Takahashi, M., & Iwakura, Y. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.187.9.1463 · Cited by 611
Watkins, L. R., Goehler, L. E., Relton, J. K., Tartaglia, N., Silbert, L., Martin, D., & Maier, S. F. (1995) · Neuroscience Letters · doi:10.1016/0304-3940(94)11105-r · Cited by 516
Givalois, L., Dornand, J., Mekaouche, M., Solier, M. D., Bristow, A. F., Ixart, G., Siaud, P., Assenmacher, I., & Barbanel, G. (1994) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.1994.267.1.r164 · Cited by 249
Breder, C. D., Hazuka, C., Ghayur, T., Klug, C., Huginin, M., Yasuda, K., Teng, M., & Saper, C. B. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.24.11393 · Cited by 226
Cited by
Understanding the symptoms of the common cold and influenza
Eccles, R. (2005) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(05)70270-x · Cited by 650
Conti, B. (2004) · Frontiers in Bioscience · doi:10.2741/1341 · Cited by 408
Fever and hypothermia in systemic inflammation: recent discoveries and revisions
Romanovsky, A. (2005) · Frontiers in Bioscience · doi:10.2741/1690 · Cited by 344
Maciag, P. C., Radulovic, S., & Rothman, J. (2009) · Vaccine · doi:10.1016/j.vaccine.2009.04.041 · Cited by 324
IL-1β/IL-6/CRP and IL-18/ferritin: Distinct Inflammatory Programs in Infections
Slaats, J., ten Oever, J., van de Veerdonk, F. L., & Netea, M. G. (2016) · PLOS Pathogens · doi:10.1371/journal.ppat.1005973 · Cited by 317
Self-citation
Metadata
- Authors
- Netea, M. G., Kullberg, B. J., & Van der Meer, J. W. M.
- Venue
- Clinical Infectious Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-10-01
- Volume
- 31
- Issue
- Supplement_5
- Pages
- S178-S184
- ISSN
- 1058-4838 (ISSN-L)
- 1537-6591
- OpenAlex
- W2045791019
- Cited by
- 357
- References
- 6
- FWCI
- 4.47
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
