Abstract
Acute stress results in local inflammation that is regulated by glucocorticoids (GCs), while chronic stress can result in systemic inflammation that is often accompanied by adverse health outcomes. Many studies have documented gender differences in the HPA axis and inflammatory stress responses contributing to different patterns of diseases susceptibilities between men and women. Women typically mount a stronger immune response to bacterial infection protecting them infectious diseases but may increase susceptibility to autoimmune disorders. Men are more susceptible to infectious diseases but are at lower risks for autoimmune disorders. Few studies have explored GC sensitivity as the primary mechanism regulating gender differences in HPA axis reactivity and inflammatory stress responses. In this study, we exposed healthy young and old male and female adults to a psychosocial stressor and studied in-vitro GC sensitivity as measured by Dexamethasone inhibition of lipopolysaccharide(LPS)-stimulated interleukin-6 (IL-6) production. We found that GC sensitivity is increased in young males compared to older males, which has been previously described. However there were no significant differences in GC sensitivities between older and younger females. Our data does not support our hypothesis that GC sensitivity is the main factor regulating the sex differences seen in neuroendocrine and inflammatory stress responses. However, the fact that GC sensitivity changes with age and cortisol in men might be a reflection of sex differences in the neuroendocrine-immune feedback loop. In women, this feedback mechanism may be less efficient contributing to a higher susceptibility to inflammatory diseases.