原创力文档do stress responses promote leukemia progression an animal study suggesting a role for epinephrine and prostaglandin-e2 through reduced nk activity做动物应激反应促进白血病进展研究显示肾上腺素的作用,通过减少prostaglandin-e2 nk活动.pdfVIP
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do stress responses promote leukemia progression an animal study suggesting a role for epinephrine and prostaglandin-e2 through reduced nk activity做动物应激反应促进白血病进展研究显示肾上腺素的作用,通过减少prostaglandin-e2 nk活动
Do Stress Responses Promote Leukemia Progression? An
Animal Study Suggesting a Role for Epinephrine and
Prostaglandin-E2 through Reduced NK Activity
. .
Shelly Inbar , Elad Neeman , Roi Avraham, Marganit Benish, Ella Rosenne, Shamgar Ben-Eliyahu*
Neuroimmunology Research Unit, Department of Psychology, Tel Aviv University, Tel Aviv, Israel
Abstract
In leukemia patients, stress and anxiety were suggested to predict poorer prognosis. Oncological patients experience ample
physiological and psychological stress, potentially leading to increased secretion of stress factors, including epinephrine,
corticosteroids, and prostaglandins. Here we tested whether environmental stress and these stress factors impact survival of
leukemia-challenged rats, and studied mediating mechanisms. F344 rats were administered with a miniscule dose of 60
CRNK-16 leukemia cells, and were subjected to intermittent forced swim stress or to administration of physiologically
relevant doses of epinephrine, prostaglandin-E2 or corticosterone. Stress and each stress factor, and/or their combinations,
doubled mortality rates when acutely applied simultaneously with, or two or six days after tumor challenge. Acute
administration of the b-adrenergic blocker nadolol diminished the effects of environmental stress, without affecting
baseline survival rates. Prolonged b-adrenergic blockade or COX inhibition (using etodolac) also increased baseline survival
rates, possibly by blocking tumor-related or normal levels of catecholamines and prostaglandins. Searching for mediating
mechanisms, we found that each of the stress factors transiently suppressed NK activity against CRNK-16 and YAC-1 lines on
a per NK basis. In contrast, the direct effects of stress factors on CRN
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