Abstract
We have previously demonstrated that central administration of interleukin (IL)-1β suppresses natural killer (NK) cell activity, impairs NK-mediated lung clearance of tumor cells, and enhances tumor colonization. The central pathways activated by IL-1β are as yet unknown. Using an in vivo model of tumor colonization, this study examined the role of central noradrenergic, opioid and prostaglandin mechanisms in mediating the effect of IL-1β on lung clearance of tumor cells. We demonstrate that central noradrenergic and opioid systems are not critically involved in this effect. Neither depletion of central noradrenergic pathways, or administration of the opioid antagonist, naltrexone (50 ug), blocked the impaired lung clearance of MADB106 tumor cells induced by central administration of IL-1β (20 ng). Central prostaglandins (PGs) do, however, appear to play a critical role. Central administration of the prostaglandin antagonist, diclofenac (250 ug), but not ibuprofen, completely blocked the effect of IL-1β on lung clearance of tumor cells. Antagonism of the effects of IL-1β was shown to be due to the effects of centrally and not of peripherally acting prostaglandins.
| Original language | English |
|---|---|
| Pages (from-to) | 57-63 |
| Number of pages | 7 |
| Journal | Journal of Neuroimmunology |
| Volume | 119 |
| Issue number | 1 |
| DOIs | |
| State | Published - 3 Sep 2001 |
Bibliographical note
Funding Information:This research was supported by The Department of Veterans Affairs Medical Research Service, NIH/NIAAA AA09850, and the US–Israel Binational Science Foundation 94-00062. We also acknowledge the generous donation of IL-1β from the National Cancer Institute (Biological Response Modifiers Program, NIH/NCI). The expert technical assistance of Mr. Ngy Heng and Khai Nguyen was also greatly appreciated.
Keywords
- Catecholamines
- IL-1β
- MADB106
- Metastasis
- NK cells
- Opioids
- Prostaglandins
- Tumor
