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Am J Physiol Regul Integr Comp Physiol 276: R1653-R1660, 1999;
0363-6119/99 $5.00
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Vol. 276, Issue 6, R1653-R1660, June 1999

Exposure to febrile temperature upregulates expression of pyrogenic cytokines in endotoxin-challenged mice

Qingqi Jiang1,2, Louis Detolla3, Ishwar S. Singh1,4, Lisa Gatdula1,4,5, Bridget Fitzgerald1,4,5, Nico van Rooijen6, Alan S. Cross7, and Jeffrey D. Hasday1,2,4,5

Divisions of 1 Pulmonary and Critical Care Medicine and 7 Infectious Disease, Departments of Medicine and 2 Pathology, and 3 Program of Comparative Medicine, University of Maryland School of Medicine, 4 Medicine and Research Services of the Baltimore Veterans Affairs Medical Center, and 5 University of Maryland at Baltimore Cytokine Core Laboratory, Baltimore, Maryland 21201; and 6 Department of Cell Biology and Immunology, Universiteit Van der Boechorststraat, 1081 BT Amsterdam, The Netherlands

Fever is a phylogenetically ancient response that is associated with improved survival in acute infections. In endothermic animals, fever is induced by a set of pyrogenic cytokines [tumor necrosis factor-alpha (TNF-alpha ), interleukin (IL)-1, and IL-6] that are also essential for survival in acute infections. We studied the influence of core temperature on cytokine expression using an anesthetized mouse model in which core temperature was adjusted by immersion in water baths. We showed that raising core temperature from basal (36.5-37.5°C) to febrile (39.5-40°C) levels increased peak plasma TNF-alpha and IL-6 levels by 4.1- and 2.7-fold, respectively, and changed the kinetics of IL-1beta expression in response to lipopolysaccharide challenge. TNF-alpha levels were increased predominantly in liver, IL-1beta levels were higher in lung, and IL-6 levels were widely increased in multiple organs in the warmer mice. This demonstrates that the thermal component of fever may directly contribute to shaping the host response by regulating the timing, magnitude, and tissue distribution of cytokine generation during the acute-phase response.

fever; body temperature; tumor necrosis factor-alpha ; interleukin-1; interleukin-6; Kupffer cells; heat shock proteins


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