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Articles in PresS, published online ahead of print December 13, 2002
J Appl Physiol, 10.1152/jap.00485.2002
Submitted on June 3, 2002
Accepted on December 11, 2002
1 Veterinary-Physiology, University of Giessen, Faculty of Veterinary Medicine, Giessen, Germany; Physiology and Pathophysiology, University of Marburg, Faculty of Medicine, Marburg, Germany
2 Veterinary-Physiology, University of Giessen, Faculty of Veterinary Medicine, Giessen, Germany
3 Physiology and Pathophysiology, University of Marburg, Faculty of Medicine, Marburg, Germany
* To whom correspondence should be addressed. E-mail: joachim.roth{at}vetmed.uni-giessen.de.
In guinea pigs, dose-dependent febrile responses can be induced by injection of a high (100 µg/kg) or a low (10 µg/kg) dose of bacterial lipopolysaccharide (LPS) into artificial subcutaneously implanted teflon chambers. In this fever model LPS does not enter the systemic circulation from the site of localized tissue inflammation in considerable amounts but causes a local induction of the proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-6 (IL-6) which can be measured in lavage fluid collected from the chamber area. Only in response to the high LPS dose small traces of TNF are measurable in blood plasma. A moderate increase of circulating IL-6 occurs in response to administration of both LPS-doses. In order to investigate the putative roles of TNF and prostaglandins (PGs) in this fever model, a neutralizing TNF binding protein (TNF-bp), or a non-selective inhibitor of cyclooxygenases (diclofenac) were injected along with the high or low dose of LPS into the subcutaneous chamber. In control groups, both doses of LPS were administered into the chamber along with the respective vehicles for the applied drugs. The fever response to the high LPS-dose remained unimpaired by treatment with TNF-bp in spite of an effective neutralization of bioactive TNF in the inflamed tissue area. In response to the low LPS-dose there was an accelerated defervescence under the influence of TNF-bp. Blockade of PG-formation with diclofenac completely abolished fever in response to both LPS doses. In conclusion, PGs seem to be essential components for the manifestation of fever in this model. While circulating TNF is known to act as a humoral pyrogenic factor, the local formation of this cytokine within inflamed subcutaneous tissue seems not to play a predominant role in the generation of a febrile response.
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