Tags

Type your tag names separated by a space and hit enter

Stress-induced changes in LPS-induced pro-inflammatory cytokine production in chronic fatigue syndrome.
Psychoneuroendocrinology. 2005 Feb; 30(2):188-98.P

Abstract

OBJECTIVE

It has been suggested that a hypofunctional hypothalamic-pituitary-adrenal (HPA) axis in chronic fatigue syndrome could result in an exaggerated release of pro-inflammatory cytokines during stress. As pro-inflammatory cytokines are involved in the induction of sickness behavior and thus constitute a potential physiological correlate of stress-induced symptom exacerbation in chronic fatigue syndrome, we set out to evaluate the LPS-induced production of pro-inflammatory cytokines during psychosocial stress in CFS and healthy controls.

METHOD

Twenty-one CFS patients and 20 healthy controls matched for age and gender underwent a standardized psychosocial stress test (Trier social stress test, TSST). Adrenocorticotropine hormone (ACTH), salivary cortisol and plasma cortisol levels were measured before and repeatedly following exposure to the stressor. Lipopolysaccharide-stimulated production of interleukin-6 and tumor necrosis factor-alpha were assessed at baseline as well as 10 and 60 min after the stress test.

RESULTS

CFS patients showed an inverse stress-induced response pattern of LPS-stimulated cytokines responses in comparison to healthy controls, i.e. stimulated cytokine production decreased shortly after stress in CFS patients, while it increased in controls. Fatigue scores and basal LPS-induced cytokine levels were significantly associated for TNF-alpha in controls and for both cytokines in CFS patients. Stress-induced changes in stimulated cytokine production were not associated with general fatigue scores in the control group, whereas in the CFS group, fatigue scores were significantly correlated with integrated levels of LPS-induced cytokines. However, partial correlations revealed that these results were due to the high correlations with basal LPS-induced cytokine levels.

CONCLUSION

CFS patients do not show an exaggerated secretion of LPS-induced cytokines. Although cortisol responses to stress were normal, pro-inflammatory cytokine levels in CFS patients were significantly attenuated. Possible intracellular mechanisms, such as for example an enhanced sensitivity to inhibitory effects of glucocorticoids, a diminished responsivity to catecholaminergic stimulation, and a disruption of intracellular activation are discussed. Basal levels of stimulated pro-inflammatory Il-6 levels are generally related to fatigue scores. However, in CFS patients this association is of greater magnitude and can also be observed for TNF-alpha.

Authors+Show Affiliations

Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany. j.gaab@psychology.unizh.chNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Controlled Clinical Trial
Journal Article

Language

eng

PubMed ID

15471616

Citation

Gaab, Jens, et al. "Stress-induced Changes in LPS-induced Pro-inflammatory Cytokine Production in Chronic Fatigue Syndrome." Psychoneuroendocrinology, vol. 30, no. 2, 2005, pp. 188-98.
Gaab J, Rohleder N, Heitz V, et al. Stress-induced changes in LPS-induced pro-inflammatory cytokine production in chronic fatigue syndrome. Psychoneuroendocrinology. 2005;30(2):188-98.
Gaab, J., Rohleder, N., Heitz, V., Engert, V., Schad, T., Schürmeyer, T. H., & Ehlert, U. (2005). Stress-induced changes in LPS-induced pro-inflammatory cytokine production in chronic fatigue syndrome. Psychoneuroendocrinology, 30(2), 188-98.
Gaab J, et al. Stress-induced Changes in LPS-induced Pro-inflammatory Cytokine Production in Chronic Fatigue Syndrome. Psychoneuroendocrinology. 2005;30(2):188-98. PubMed PMID: 15471616.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Stress-induced changes in LPS-induced pro-inflammatory cytokine production in chronic fatigue syndrome. AU - Gaab,Jens, AU - Rohleder,Nicolas, AU - Heitz,Vera, AU - Engert,Veronika, AU - Schad,Tanja, AU - Schürmeyer,Thomas H, AU - Ehlert,Ulrike, PY - 2004/03/18/received PY - 2004/06/11/revised PY - 2004/06/12/accepted PY - 2004/10/9/pubmed PY - 2005/1/26/medline PY - 2004/10/9/entrez SP - 188 EP - 98 JF - Psychoneuroendocrinology JO - Psychoneuroendocrinology VL - 30 IS - 2 N2 - OBJECTIVE: It has been suggested that a hypofunctional hypothalamic-pituitary-adrenal (HPA) axis in chronic fatigue syndrome could result in an exaggerated release of pro-inflammatory cytokines during stress. As pro-inflammatory cytokines are involved in the induction of sickness behavior and thus constitute a potential physiological correlate of stress-induced symptom exacerbation in chronic fatigue syndrome, we set out to evaluate the LPS-induced production of pro-inflammatory cytokines during psychosocial stress in CFS and healthy controls. METHOD: Twenty-one CFS patients and 20 healthy controls matched for age and gender underwent a standardized psychosocial stress test (Trier social stress test, TSST). Adrenocorticotropine hormone (ACTH), salivary cortisol and plasma cortisol levels were measured before and repeatedly following exposure to the stressor. Lipopolysaccharide-stimulated production of interleukin-6 and tumor necrosis factor-alpha were assessed at baseline as well as 10 and 60 min after the stress test. RESULTS: CFS patients showed an inverse stress-induced response pattern of LPS-stimulated cytokines responses in comparison to healthy controls, i.e. stimulated cytokine production decreased shortly after stress in CFS patients, while it increased in controls. Fatigue scores and basal LPS-induced cytokine levels were significantly associated for TNF-alpha in controls and for both cytokines in CFS patients. Stress-induced changes in stimulated cytokine production were not associated with general fatigue scores in the control group, whereas in the CFS group, fatigue scores were significantly correlated with integrated levels of LPS-induced cytokines. However, partial correlations revealed that these results were due to the high correlations with basal LPS-induced cytokine levels. CONCLUSION: CFS patients do not show an exaggerated secretion of LPS-induced cytokines. Although cortisol responses to stress were normal, pro-inflammatory cytokine levels in CFS patients were significantly attenuated. Possible intracellular mechanisms, such as for example an enhanced sensitivity to inhibitory effects of glucocorticoids, a diminished responsivity to catecholaminergic stimulation, and a disruption of intracellular activation are discussed. Basal levels of stimulated pro-inflammatory Il-6 levels are generally related to fatigue scores. However, in CFS patients this association is of greater magnitude and can also be observed for TNF-alpha. SN - 0306-4530 UR - https://www.unboundmedicine.com/medline/citation/15471616/Stress_induced_changes_in_LPS_induced_pro_inflammatory_cytokine_production_in_chronic_fatigue_syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4530(04)00119-2 DB - PRIME DP - Unbound Medicine ER -