STRESSOR-INDUCED ALTERATION OF CYTOKINE PRODUCTION IN MULTIPLE-SCLEROSIS PATIENTS AND CONTROLS

Citation
Kd. Ackerman et al., STRESSOR-INDUCED ALTERATION OF CYTOKINE PRODUCTION IN MULTIPLE-SCLEROSIS PATIENTS AND CONTROLS, Psychosomatic medicine, 60(4), 1998, pp. 484-491
Citations number
77
Categorie Soggetti
Psychology,Psychiatry,Psychiatry,Psychology
Journal title
ISSN journal
00333174
Volume
60
Issue
4
Year of publication
1998
Pages
484 - 491
Database
ISI
SICI code
0033-3174(1998)60:4<484:SAOCPI>2.0.ZU;2-2
Abstract
Objective: We administered an acute psychological stressor to multiple sclerosis (MS) patients and normal controls to determine whether diff erences in subjective and physiological responses to stress may underl ie the susceptibility of MS patients to stress-related exacerbations. Method: Twenty-five MS patients (18 female, 7 male) and 25 age- and Se nder-matched controls participated in the study. They were asked to gi ve a 5-minute videotaped speech defending themselves in a hypothetical scenario in which they were wrongly accused of stealing. Subjective a nd autonomic responses were monitored, and blood was sampled at baseli ne, 5, 20, and 60 minutes after the stressor to assess mitogen-stimula ted production of interleukin-1 beta (IL-1 beta), interleukin-4 (IL-4) , tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-g amma). Results: MS patients and controls demonstrated similar subjecti ve and physiological responses to the stressor that were independent o f gender, mood, and disability status. The macrophage-derived cytokine s IL-1 beta and TNF-alpha were increased during the stressor, and rema ined elevated through 60 minutes. Th1 lymphocyte-derived IFN-gamma pro duction also was increased at 5 and 60 minutes relative to baseline; h owever, there was no change in the Th2 lymphocyte-derived cytokine IL- 4. Conclusions: These results favor the hypothesis that MS patients do not differ in stress response from normal controls; however, psycholo gical stress may enhance cellular immune responses that would be poten tially harmful to MS patients.