Acute phase protein, serum amyloid A, inhibits IL-1- and TNF-induced fever and hypothalamic PGE2 in mice.
The effect of serum amyloid A (SAA) on fever induced by recombinant interleukin-1 beta (rIL-1 beta) or recombinant tumour necrosis factor alpha (rTNF alpha) was studied in mice. Serum amyloid A is an acute phase protein whose rise in pathological events is induced by the cytokines IL-1, IL-6 and TNF. Administration of human serum amyloid A to mice inhibited fever induced by rIL-1 beta or rTNF alpha in vivo, while the addition of human serum amyloid A to mice hypothalamic slices inhibited IL-1 beta- or TNF alpha-induced prostaglandin E2 (PGE2) production in vitro. Since serum amyloid A did not affect body temperature or hypothalamic PGE2 levels when administered alone, it may represent a specific servo-mechanism for fever regulation in acute events, and it suggests, for the first time, a possible feedback relationship between serum amyloid A and the immunoregulatory cytokines.
Shainkin-Kestenbaum
R
R
Sapir Medical Center, Meir Hospital, Kfar-Saba, Israel.
Berlyne
G
G
Zimlichman
S
S
Sorin
H R
HR
Nyska
M
M
Danon
A
A
D000209:Acute-Phase Proteins / Q000494:pharmacology*; D000818:Animals; D015232:Dinoprostone / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D005334:Fever / Q000209:etiology*; D007031:Hypothalamus / Q000378:metabolism*; D066298:In Vitro Techniques; D007375:Interleukin-1 / Q000037:antagonists & inhibitors*; D051379:Mice; D000685:Serum Amyloid A Protein / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D000209:Acute-Phase Proteins; D007375:Interleukin-1; D000685:Serum Amyloid A Protein; D014409:Tumor Necrosis Factor-alpha; D015232:Dinoprostone