Behavioral characteristics closely associated with specific physiological profiles present an important area of research in understanding health disparities. In particular, glucocorticoid overproduction may be an important factor moderating disease progression; natural variance in production of this steroid has been proposed as one mechanism underlying individual differences in health and disease. In the current paper, we examined immune parameters in female rats of two different behavioral types previously shown to have differential glucocorticoid production and life spans. We categorized young female rats according to their behavioral response to novelty (high- or low-locomotion), and compared their glucocorticoid production, adrenal size, thymus size, tumor necrosis factor-α (TNF-α) production, tumor development and life span. As expected, high-locomotion females produced more glucocorticoids and had larger adrenal glands during young adulthood than did low-locomotion females. High-locomotion females had significantly smaller thymuses and reduced TNF-α levels compared to low-locomotion, suggesting altered immune function in young adulthood. Finally, high-locomotion females had shorter life spans than did low-locomotion females, and this was particularly true in females that developed pituitary tumors, but not in those that developed mammary tumors. These results, along with other published findings, suggest that high-locomotion rodent females experience life-long elevations in glucocorticoid responses to novelty, and that these elevated levels may be comparable to chronic stress. This naturally occurring endocrine profile may influence immune responses which in turn could affect disease susceptibility. Variance in immune function across personality types may be partially moderated by natural variance in glucocorticoid production.
Bibliographical noteFunding Information:
We thank A.C. Ross and J.F. Sheridan for advice on possible immune measures, and R. Anolik, C. Barrett, A. Bruscke, M. Diep, K. Haskins, A. Jefferson, C. Kovacsics, C. Mateo, J. McGovern, and K. Mehta, J. Quinn, and R. Smull for expert assistance with data collection. This research was supported by NIMH R03 MH071406 (SAC) and internal Pennsylvania State University Funding (S.A.C. and L.C.K.).
- Life span
- Pro-inflammatory cytokines
- Tumor development
- Tumor necrosis factor α