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Afferent pathways of pyrogen signaling
Clark M Blatteis1, Elmir Sehic1, Shuxin Li1
1Department of Physiology and Biophysics, The University of Tennessee, Memphis, Memphis, Tennessee 38163, USA.
Annals of the New York Academy of Sciences
|January 26, 1999
Summary
Lipopolysaccharide (LPS) fever involves liver cells and the complement system. Disabling Kupffer cells (Kc) reduced fever, suggesting their role in initiating LPS-induced fever responses.
Area of Science:
- Immunology
- Neuroscience
- Physiology
Background:
- Fever induced by lipopolysaccharide (LPS) may involve brain signaling through hepatic vagal afferents.
- This suggests liver-derived mediators, potentially from Kupffer cells (Kc), initiate LPS fever.
Purpose of the Study:
- To investigate the role of Kupffer cells (Kc) in initiating LPS-induced fever.
- To explore the involvement of the complement system in LPS fever.
Main Methods:
- Kc were disabled in conscious guinea pigs using gadolinium chloride.
- Core body temperature and preoptic prostaglandin E2 (PGE2) were monitored following intravenous LPS administration.
- Guinea pigs were hypocomplemented using cobra venom factor to assess complement system involvement.
Main Results:
- Gadolinium chloride pretreatment significantly attenuated both fever and PGE2 responses to LPS.
- Fluorescein-labeled LPS was detected in Kc, but also in pretreated animals.
- Complement depletion (>60%) reduced LPS-induced fever, and LPS administration consumed complement (~12% within 10 minutes).
Conclusions:
- Kc activation appears to be involved in LPS fever onset.
- The complement system also plays a role in LPS fever.
- The precise roles of Kc and complement in LPS fever require further clarification.