Publication Date:
1989-02-24
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davatelis, G -- Wolpe, S D -- Sherry, B -- Dayer, J M -- Chicheportiche, R -- Cerami, A -- AI121359/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1989 Feb 24;243(4894 Pt 1):1066-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2646711" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Chemotactic Factors/isolation & purification/*physiology
;
Dinoprostone/physiology
;
Female
;
Fever/*chemically induced
;
Heparin/metabolism
;
Humans
;
Ibuprofen/pharmacology
;
Interleukin-1/physiology
;
Interleukin-8
;
Neutrophils/physiology
;
Rabbits
;
Recombinant Proteins
;
Tumor Necrosis Factor-alpha/physiology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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