Effect of Gender and Menstrual Cycle on Immune System Response to Acute Mental Stress: Apoptosis as a Mediator


PEHLİVANOĞLU B. , BAYRAK S. , GUREL E. I. , BALKANCI Z. D.

NEUROIMMUNOMODULATION, cilt.19, sa.1, ss.25-32, 2012 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 19 Konu: 1
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1159/000327993
  • Dergi Adı: NEUROIMMUNOMODULATION
  • Sayfa Sayıları: ss.25-32

Özet

Background/Aims: We aimed to explore the immunological outcomes of short-term mental stress in apoptosis in peripheral lymphocytes and variations by gender and hormonal status of the individuals together with possible mediators of this interaction. Methods: Acute mental stress (computerized Stroop color-word interference and cold pressor tests) was applied to men (n = 17) and women (n = 16, in both follicular and luteal phases). Heart rate and blood pressure were monitored throughout the test and after the test until baseline values were recorded. Blood samples were drawn for measuring cortisol and nitric oxide (NO) levels and flow-cytometric cell counting before and after the test. Results: Activation of the stress system was ascertained by increased heart rate, blood pressure and serum cortisol levels after the test. Relative to baseline values, acute mental stress altered the distribution of T and natural killer cells. There was a significant decrease in T helper/T cytotoxic-suppressor cell ratio and an increase in apoptotic T helper cell percentage irrespective of gender or menstrual cycle phase. An increased number of natural killer cells was detected in women, whereas it was decreased in men. After stress induction, serum NO levels remained the same in women and increased in men. Although a correlation was not found between immune system changes and NO levels, glucocorticoids seem to have a role in the observed differences. Conclusion: Acute mental stress triggers apoptotic T helper cell loss which was associated with stress system activation, and sex steroids affect the pattern of stress-related immune cell distribution. Copyright (C) 2011 S. Karger AG, Basel