Blunted affect is associated with hypothalamic--pituitary--adrenal axis (HPA) hypoactivity and elevated CSF-interleukin-1 beta (IL-1β) in response to lumbar puncture.
OBJECTIVE
Proinflammatory activity has been suggested as one of the psychophysiological mechanisms responsible for the health risks associated with stress and mood disorders. There have been limited studies evaluating central immune and hypothalamic- pituitary-adrenal (HPA) axis responses to experimental stress in healthy women. The current study compared, under a controlled condition, the baseline measures and biological and psychological responses to a physical stressor (lumbar puncture [LP]) of healthy women who exhibited an abnormal serum cortisol response (nonresponders [NRs]) to the LP to those of normal controls (responders [Rs]), allowing assessment of stress responsivity and the functional integrity of the feedback system of the HPA axis, sympathetic nervous system (SNS), and neuroimmune axis.


METHODS
Serum adrenocorticotropic hormone (ACTH), cortisol, interleukin (IL)-6, IL-1sR, and central IL-1β, IL-6, norepineprhine (NE), corticotropin-releasing factor (CRF), and affective states (using the Stress Symptom Rating Questionnaire) were measured in five NRs and seven Rs.


RESULTS
Compared with NR subjects, Rs had significantly higher levels of ACTH and central IL-1β, higher ratings of attention, and lower perceived stress and anxiety. There were no differences between the groups in serum cortisol, IL-6, or IL-1sR or in central IL-6, NE, and CRF.


CONCLUSIONS
Women with significantly elevated IL-1β (NRs) responded to an extreme physical stressor with an attenuated HPA system and abnormal subjective ratings compared to healthy women with lower values of central IL-1β. These findings support the suppression of the effects of HPA-axis cortisol on proinflammatory cytokine production. It is possible that these differences in the psychoneuroimmunological profiles of NRs will lead to increased psychobiological vulnerability and predict future health risk.
University of California, Los Angeles, School of Nursing, Los Angeles, CA, USA. lfitzger@sonnet.ucla.edu
Leah
L
Fitzgerald
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D053583:Interleukin-1beta / Q000134:cerebrospinal fluid*; D010913:Pituitary-Adrenal System / Q000502:physiology*; D013129:Spinal Puncture; D011795:Surveys and Questionnaires
D016207:Cytokines; D053583:Interleukin-1beta; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone