Intracerebral interleukin-1β impairs response to tumor invasion: Involvement of adrenal catecholamines

Deborah M. Hodgson*, Raz Yirmiya, Francesco Chiappelli, Anna N. Taylor

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


Interleukin-1β (IL-1β) is released within the brain following stress, trauma, infection, and in specific brain disorders. This centrally acting IL- 1β has recently been shown to impair peripheral immunity. Central administration of IL-1β suppresses natural killer (NK) cell activity impairs lung clearance of tumor cells and enhances tumor colonization. Using an in vivo model of tumor colonization (lung clearance of NK-sensitive MADB106 adenocarcinoma cells), this study examined the role of the hypothalamic- pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) in mediating these effects. We demonstrate that adrenalectomy significantly attenuated the impaired lung clearance of MADB106 tumor cells induced by intracerebroventricular (i.c.v.) administration of IL-1β (20 ng). Supplementing adrenalectomized animals with corticosterone did not reinstate the effect. The effect of IL-1β on lung clearance was blocked by pretreatment with the β-adrenergic antagonist, nadolol (0.5 mg/kg), but not by the α-antagonist phentolamine (5 mg/kg). Peripheral noradrenergic pathways are not implicated given that systemic administration of the noradrenergic neurotoxin, 6-hydroxy-dopamine, did not block the effect of IL- 1β. Taken together, these findings indicate that IL-1β impairs lung clearance of MADB106 tumor cells via the actions of adrenal catecholamines, most likely epinephrine, acting at β-adrenergic receptors in the periphery.

Original languageAmerican English
Pages (from-to)200-208
Number of pages9
JournalBrain Research
Issue number1
StatePublished - 16 Jan 1999

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, and the facilities provided by Prof. Donald Novin were also greatly appreciated.


  • Catecholamine
  • IL-1
  • MADB106
  • NK cell
  • Tumor


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