Stress increases metastatic spread of a mammary tumor in rats: Evidence for mediation by the immune system

S. Ben-Eliyahu*, R. Yirmiya, J. C. Liebeskind, A. N. Taylor, R. P. Gale

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

215 Scopus citations

Abstract

Causal relationships among stress, immune suppression, and enhanced tumor development have often been suggested, but direct evidence is scant. We studied stress effects in Fischer 344 rats using a tumor model in which lung metastases of a syngeneic mammary tumor (MADB106) are controlled by natural killer (NK) cells. Animals exposed to acute stress showed a substantial decrease in NK cell cytotoxicity against this tumor in an in vitro assay and, when intravenously injected with this tumor, showed a twofold increase in surface lung metastases. The critical period during which stress increases metastases appears to be the same as that during which this tumor is known to be controlled by NK cells. These findings support the hypothesis that stress can facilitate the metastatic process via suppression of the immune system.

Original languageAmerican English
Pages (from-to)193-205
Number of pages13
JournalBrain, Behavior, and Immunity
Volume5
Issue number2
DOIs
StatePublished - Jun 1991

Bibliographical note

Funding Information:
We dedicate this paper to Mr. Norman Cousins whose kindness and encouragement was a continuing inspiration. This research was supported by NIH Grant NS 07628, the David H. Murdock Foundation for Advanced Brain Studies, and an Unrestricted Pain Research Grant from the Bristol-Myers Squibb Co. (J.C.L.) and by a grant from the VA Medical Research Service (A.N.T.). S.B.-E. and R.Y. were supported by the UCLA Task Force on Psychoneuroimmunology.

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