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Infection and Immunity, April 1999, p. 1539-1546, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Febrile-Range Temperature Modifies Early Systemic Tumor Necrosis Factor Alpha Expression in Mice Challenged with Bacterial Endotoxin

Qingqi Jiang,1,2 Louis DeTolla,3 Nico van Rooijen,4 Ishwar S. Singh,1 Bridget Fitzgerald,1,5 Michael M. Lipsky,2 Andrew S. Kane,2 Alan S. Cross,6 and Jeffrey D. Hasday1,2,5,7,*

Division of Pulmonary and Critical Care Medicine1 and Division of Infectious Disease,6 Department of Medicine, Department of Pathology,2 and Program of Comparative Medicine,3 University of Maryland School of Medicine, UMAB Cytokine Core Laboratory,5 and Medicine and Research Services of the Baltimore VA Medical Center,7 Baltimore, Maryland 21201, and Department of Cell Biology and Immunology, Vrije Universiteit, Amsterdam, The Netherlands4

Received 20 July 1998/Returned for modification 5 October 1998/Accepted 25 November 1998

Fever improves survival in acute infections, but the effects of increased core temperature on host defenses are poorly understood. Tumor necrosis factor alpha (TNF-alpha ) is an early activator of host defenses and a major endogenous pyrogen. TNF-alpha expression is essential for survival in bacterial infections but, if disregulated, can cause tissue injury. In this study, we show that passively increasing core temperature in mice from the basal (36.5 to 37.5°C) to the febrile (39.5 to 40°C) range modifies systemic TNF-alpha expression in response to bacterial endotoxin (lipopolysaccharide). The early TNF-alpha secretion rate is enhanced, but the duration of maximal TNF-alpha production is shortened. We identified Kupffer cells as the predominant source of the excess TNF-alpha production in the warmer animals. The enhanced early TNF-alpha production observed at the higher temperature in vivo could not be demonstrated in isolated Kupffer cells or in precision-cut liver slices in vitro, indicating the participation of indirect pathways. Therefore, expression of the endogenous pyrogen TNF-alpha is regulated by increments in core temperature during fever, generating an enhanced early, self-limited TNF-alpha pulse.

* Corresponding author. Mailing address: 10 N. Greene St., Rm. 3D127, Baltimore, MD 21201. Phone: 410-605-7197. Fax: 410-605-7915. E-mail: jhasday{at}umaryland.edu.

Infection and Immunity, April 1999, p. 1539-1546, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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