| Autor: |
Li, Mary H., Seatter, Susan C., Manthei, Robin, Bubrick, Melvin, West, Michael A. |
| Zdroj: |
Journal of Surgical Research; July 1994, Vol. 57 Issue: 1 p85-92, 8p |
| Abstrakt: |
Macrophages pretreated with low-dose endotoxin [lipopolysaccharide (LPS1)] have an altered response to subsequent endotoxin (LPS2) stimulation, a process known as endotoxin tolerance. In this study we investigated whether the LPS1pretreatment effects were mediated primarily via tumor necrosis factor (TNFα). Murine peritoneal macrophages were pretreated in vitrowith either TNFα or LPS1and the effects on mediator production in response to a second endotoxin exposure, LPS2, were compared. Mediators in macrophage supernatant were measured using specific bioassays [TNF, interleukin-1 (IL-1), and IL-6] or enzymatic immunoassays [prostaglandin E2(PGE2) and TNF]. Macrophage production of all mediators was stimulated by endotoxin in the absence of LPS1pretreatment. Pretreatment with LPS1completely inhibited LPS2-triggered TNF release whereas preexposure to TNFα had no effect. In contrast, LPS1pretreatment significantly augmented IL-1 and PGE2release in response to LPS2, whereas pretreatment using either high- or low dose TNFα did not. TNF, stimulated by an initial exposure to endotoxin, LPS1, is not solely responsible for the observed alterations in macrophage mediator release following a subsequent endotoxin stimulus (LPS2). Thus, the data suggest that endotoxin tolerance is mediated primarily by factors other than TNF. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
