| Autor: |
O'Grady NP; National Institutes of Health, Warren Grant Magnuson Clinical Center, Building 10, Rm 7D-43, 10 Center Drive, MSC-1662, Bethesda, MD 20892- 1662, USA. nogrady@cc.nih.gov, Tropea M, Preas HL 2nd, Reda D, Vandivier RW, Banks SM, Suffredini AF |
| Jazyk: |
angličtina |
| Zdroj: |
The Journal of infectious diseases [J Infect Dis] 1999 Jan; Vol. 179 (1), pp. 136-41. |
| DOI: |
10.1086/314559 |
| Abstrakt: |
Macrophage inflammatory protein (MIP)-1alpha and MIP-1beta regulate leukocyte activation and trafficking. To assess the role of MIP-1alpha and MIP-1beta in human inflammation, healthy subjects were studied during experimental endotoxemia with prior administration of ibuprofen, a cyclooxygenase inhibitor, or dimeric p75 tumor necrosis factor (TNF)-alpha receptor, a TNF antagonist; septic patients were also studied. Following endotoxin, blood levels of both MIP-1 molecules rose acutely and fell to baseline by 6 h (P=. 001). While MIP-1 mediates fever in animals independent of cyclooxygenase blockade, in subjects given endotoxin and ibuprofen, MIP-1 levels increased and fever was suppressed. MIP-1 levels were not diminished by inhibiting circulating TNF-alpha in humans. In septic patients, elevated levels of MIP-1alpha and MIP-1beta were detected within 24 h of sepsis and fell in parallel with TNF-alpha and interleukin-6 (P<.01). MIP-1alpha and MIP-1beta increase during acute inflammation but are not associated with fever in endotoxemic humans during cyclooxygenase blockade. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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