Macrophage inflammatory protein-1: a prostaglandin-independent endogenous pyrogen.
Macrophage inflammatory protein-1 (MIP-1) produced a monophasic fever of rapid onset whose magnitude was equal to or greater than that of fevers produced with either recombinant human cachectin (or tumor necrosis factor) or recombinant human interleukin-1. However, in contrast to these two endogenous pyrogens, the fever induced by MIP-1 was not inhibited by the cyclooxygenase inhibitor ibuprofen. Thus, MIP-1 may participate in the febrile response that is not mediated through prostaglandin synthesis and clinically cannot be ablated by cyclooxygenase inhibitors.
Davatelis
G
G
Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.
Wolpe
S D
SD
Sherry
B
B
Dayer
J M
JM
Chicheportiche
R
R
Cerami
A
A
D000818:Animals; D002630:Chemotactic Factors / Q000302:isolation & purification / Q000502:physiology*; D015232:Dinoprostone / Q000502:physiology; D005260:Female; D005334:Fever / Q000139:chemically induced*; D006493:Heparin / Q000378:metabolism; D006801:Humans; D007052:Ibuprofen / Q000494:pharmacology; D007375:Interleukin-1 / Q000502:physiology; D016209:Interleukin-8; D009504:Neutrophils / Q000502:physiology; D011817:Rabbits; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D002630:Chemotactic Factors; D007375:Interleukin-1; D016209:Interleukin-8; D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha; D006493:Heparin; D015232:Dinoprostone; D007052:Ibuprofen