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Infection and Immunity, May 2002, p. 2519-2525, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2519-2525.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Modulation of Mouse Endotoxic Fever by Complement

S. Li,1 V. M. Holers,2 S. A. Boackle,2 and C. M. Blatteis1*

Department of Physiology, The University of Tennessee Health Science Center, Memphis, Tennessee 38163,1 Department of Medicine, University of Colorado Health Science Center, Denver, Colorado 802622

Received 2 October 2001/ Returned for modification 18 December 2001/ Accepted 31 January 2002

It was recently reported that the complement system may be critically involved in the febrile response of guinea pigs to systemic, particularly intraperitoneally (i.p.) injected, lipopolysaccharides (LPS). The present study was designed to identify which component(s) of the complement cascade may be specifically critical. To this end, we used mice with C3, C5, and CR2 gene deletions. To assess preliminarily the suitability of mice for such a study, we replicated our earlier studies with guinea pigs. Thus, to verify initially whether complement is similarly involved in the febrile response of wild-type (C57BL/6J) mice to i.p. LPS (Escherichia coli, 1 µg/mouse), we depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]). These animals did not develop fever, whereas the core temperature (Tc) of CVF vehicle-treated controls rose ~1°C by 80 min postinjection and then gradually abated over the following 2.5 h, confirming the involvement of complement in fever production after i.p. LPS injection and the suitability of this species for these studies. C3- and C5-sufficient (C3+/+ and C5+/+) mice also developed 1°C fevers within 80 min after i.p. LPS (1 or 2 µg/mouse) injection. These fevers were totally prevented by CVF (10 U/mouse, i.v.) pretreatment. C3- and C5-deficient (C3-/- and C5-/-) mice were also unable to develop Tc rises after i.p. LPS. Both CR2+/+ and CR2-/- mice responded normally to i.p. LPS (1 µg/mouse). These data indicate that C5, but not C3d acting through CR2, may play a critical role in the febrile response of mice to i.p. LPS.

* Corresponding author. Mailing address: Department of Physiology, The University of Tennessee Health Science Center, 894 Union Ave., Memphis, TN 38163. Phone: (901) 448-5845. Fax: (901) 448-7126. E-mail: blatteis{at}physio1.utmem.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, May 2002, p. 2519-2525, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2519-2525.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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