Journal
BRAIN BEHAVIOR AND IMMUNITY
Volume 21, Issue 3, Pages 251-258Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2006.08.001
Keywords
breast cancer; fatigue; inflammation; HPA axis; stress
Categories
Funding
- NCI NIH HHS [K07 CA90407] Funding Source: Medline
- NCRR NIH HHS [M01 RR00865] Funding Source: Medline
- NIAID NIH HHS [R01 AI052737] Funding Source: Medline
- NIMH NIH HHS [MH019925] Funding Source: Medline
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Fatigue is a common problem following cancer treatment and our previous studies suggest that a chronic inflammatory process might contribute to cancer-related fatigue. However, immune responses to challenge have not yet been evaluated among individuals with cancer-related fatigue, and it is not known what mechanisms drive increased levels of inflammatory markers in fatigued cancer survivors. We have previously reported that fatigued breast cancer survivors show a blunted cortisol response to an experimental psychological stressor. In this report.. we focus on inflammatory responses to this stressor and their relationship to circulating glucocorticoids and cellular sensitivity to glucocorticoid inhibition. Relative to non-fatigued control survivors, participants experiencing persistent fatigue showed significantly greater increases in LPS-stimulated production of IL-1 beta and IL-6 following the stressor (Group x Time interaction: p <.05). Fatigued participants did not show any difference in cellular sensitivity to cortisol inhibition of cytokine production, but they did show significantly less salivary cortisol increase in the aftermath of the stressor. Moreover, blunted cortisol responses were associated with significantly increased production of IL-6 in response to LPS stimulation (p <.05). These data provide further evidence of enhanced inflammatory processes in fatigued breast cancer survivors and suggest that these processes may stem in part from decreased glucocorticoid response to stress. (c) 2006 Elsevier Inc. All rights reserved.
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