Davatelis G, Wolpe S D, Sherry B, Dayer J M, Chicheportiche R, Cerami A
Laboratory of Medical Biochemistry, Rockefeller University, New York, NY 10021.
Science. 1989 Feb 24;243(4894 Pt 1):1066-8. doi: 10.1126/science.2646711.
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.
巨噬细胞炎性蛋白-1(MIP-1)可引发快速起病的单相发热,其发热程度等于或高于重组人恶病质素(或肿瘤坏死因子)或重组人白细胞介素-1所引起的发热。然而,与这两种内源性致热原不同,MIP-1诱导的发热不受环氧化酶抑制剂布洛芬的抑制。因此,MIP-1可能参与了并非通过前列腺素合成介导的发热反应,临床上不能通过环氧化酶抑制剂消除。