Stress and trauma-associated immunological changes and their implications on health
Chronischer und traumatischer Stress, wie er von Personen erlebt wurde, die unter einer Posttraumatischen Belastungsstörung (PTSD) leiden, ist assoziiert mit schlechter körperlicher Gesundheit, erhöhter Inanspruchnahme medizinischer Leistungen, und erhöhtem Risiko für eine Vielzahl körperlicher Erkrankungen wie kardiovaskuläre, inflammatorische und Autoimmunerkrankungen. Stress steht zudem im Zusammenhang mit einer erhöhten Mutagenese und einer verminderten DNA-Reparatur-Fähigkeit und damit mit einem erhöhten Risiko für Krebs. Zusammenfassend zeigen PTSD-Patienten eine hohe Morbidität und ein hohes Risiko für die Entwicklung einer Vielzahl von körperlichen Erkrankungen. Ziel dieses Projekts ist es, die Beziehung zwischen der Schwere eines Stressors und den assoziierten immunologischen Veränderungen genauer zu beleuchten sowie die funktionellen Implikationen der beobachteten immunologischen Veränderungen für die physische Gesundheit zu untersuchen.
- FB Psychologie
- Zukunftskolleg1
(2010): The Risk of Posttraumatic Stress Disorder After Trauma Depends on Traumatic Load and the Catechol-O-Methyltransferase Val158Met Polymorphism Biological Psychiatry. 2010, 67(4), pp. 304-308. Available under: doi: 10.1016/j.biopsych.2009.10.009 |
Background Forschungszusammenhang (Projekte) |
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(2010): Association Study of Trauma Load and SLC6A4 Promoter Polymorphism in Posttraumatic Stress Disorder : Evidence From Survivors of the Rwandan Genocide Journal of Clinical Psychiatry. 2010, 71(5), pp. 543-547. Available under: doi: 10.4088/JCP.08m04787blu |
Objective: As exposure to different types of traumatic stressors increases, the occurrence of posttraumatic stress disorder (PTSD) increases. However, because some people exhibit either surprising resilience or high vulnerability, further influencing factors have been conjectured, such as gene-environment interactions. The SLC6A4 gene, which encodes serotonin transporter, has been identified as predisposing toward differential emotional processing between genotypes of its promoter polymorphism. Forschungszusammenhang (Projekte) |
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(2009): Traumatisierte Therapeuten? : Ein Überblick über sekundäre Traumatisierung Zeitschrift für Klinische Psychologie & Psychotherapie. 2009, 38(4), pp. 250-261. Available under: doi: 10.1026/1616-3443.38.4.250 |
dc.title: dc.contributor.author: Kolassa, Iris-Tatjana; Jurisch, Florentine; Elbert, Thomas Forschungszusammenhang (Projekte) |
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(2009): No PTSD-related differences in diurnal cortisol profiles of genocide survivors Psychoneuroendocrinology. 2009, 34(4), pp. 523-531. Available under: doi: 10.1016/j.psyneuen.2008.10.012 |
Posttraumatic stress disorder (PTSD) has been associated with reduced cortisol levels. Opposing results have been interpreted as resulting from methodological differences between studies.We investigated the diurnal profile of salivary cortisol in a population of highly traumatized adult males from Rwanda with and without PTSD, who spent the whole day of examination together under amaximally standardized schedule. Besides the detection of PTSDrelated alterations in cortisol release we aimed at determining physiologically relevant effects of cumulative trauma exposure on HPA functioning in interaction with or independent of diagnosis. There were no differences in the diurnal pattern of cortisol release between subjects with and without PTSD. We observed an increasing prevalence of PTSD with increasing number of different traumatic event types experienced, replicating earlier results on a building-block effect of multiple traumatization. However, size of cumulative exposure was not related to any of the cortisol measures. The results suggest that besides methodological constraints also confounding factors not previously controlled for, e.g., sex differences or current life stress, might contribute to the diverging results of lowered, unchanged or enhanced cortisol secretion in PTSD. Future research should therefore closely monitor these possible confounds to optimize models for cortisol in research on stress-dependent illnesses. Forschungszusammenhang (Projekte) |
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(2009): Substantial reduction of naïve and regulatory T cells following traumatic stress Brain, Behavior, and Immunity. 2009, 23(8), pp. 1117-1124. ISSN 0889-1591. eISSN 1090-2139. Available under: doi: 10.1016/j.bbi.2009.07.003 |
Posttraumatic stress disorder (PTSD) is associated with an enhanced susceptibility to various somatic diseases. However, the exact mechanisms linking traumatic stress to subsequent physical health problems have remained unclear. This study investigated peripheral T lymphocyte differentiation subsets in 19 individuals with war and torture related PTSD compared to 27 non-PTSD controls (n = 14 traumaexposed controls; n = 13 non-exposed controls). Peripheral T cell subpopulations were classified by their characteristic expression of the lineage markers CD45RA and CCR7 into: naïve (CD45RA+ CCR7+), central memory (TCM: CD45RA- CCR7+) and effector memory (TEM: CD45RA- CCR7- and TEMRA: CD45RA- CCR7-) cells. Furthermore, we analyzed regulatory T cells (CD4+CD25+FoxP3+) and ex vivo proliferation responses of peripheral blood mononuclear cells after stimulation with anti-CD3 monoclonal antibody. Results show that the proportion of naïve CD8+ T lymphocytes was reduced by 32% (p = 0.01), whereas the proportions of CD3+ central (p = 0.02) and effector (p = 0.01) memory T lymphocytes were significantly enhanced (+22% and +34%, respectively) in PTSD patients compared to non-PTSD individuals. To a smaller extent, this effect was also observed in trauma-exposed non-PTSD individuals, indicating a cumulative effect of traumatic stress on T cell distribution. Moreover, PTSD patients displayed a 48% reduction in the proportion of regulatory T cells (p < 0.001). Functionally, these alterations were accompanied by a significantly enhanced (+34%) ex vivo proliferation of anti-CD3 stimulated T cells (p = 0.05). The profoundly altered composition of the peripheral T cell compartment might cause a state of compromised immune responsiveness, which may explain why PTSD patients show an increased susceptibility to infections, and inflammatory and autoimmune diseases. |
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(2007): A deletion variant of the alpha2b-adrenoceptor is related to emotional memory in Europeans and Africans Nature Neuroscience. 2007, 10(9), pp. 1137-1139. ISSN 1097-6256. eISSN 1546-1726. Available under: doi: 10.1038/nn1945 |
Emotionally arousing events are recalled better than neutral events. This phenomenon, which helps us to remember important and potentially vital information, depends on the activation of noradrenergic transmission in the brain. Here we show that a deletion variant of ADRA2B, the gene encoding the a2b-adrenergic receptor, is related to enhanced emotional memory in healthy Swiss subjects and in survivors of the Rwandan civil war who experienced highly aversive emotional situations. Forschungszusammenhang (Projekte) |
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(2007): Altered oscillatory brain dynamics after repeated traumatic stress BMC Psychiatry. 2007, 7(1), 56. eISSN 1471-244X. Available under: doi: 10.1186/1471-244X-7-56 |
Background: Forschungszusammenhang (Projekte) |
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(2007): Lack of cortisol response in patients with posttraumatic stress disorder (PTSD) undergoing a diagnostic interview BMC Psychiatry. 2007, 7(1), 54. eISSN 1471-244X. Available under: doi: 10.1186/1471-244X-7-54 |
Background Forschungszusammenhang (Projekte) |
Name | Kennziffer | Beschreibung | Laufzeit |
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Emmy-Noether-Programm | 427/09 | Emmy-Noether-Nachwuchsförderung |
Laufzeit: | 04.12.2008 – 04.12.2013 |