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      Effects of the Trier Social Stress Test on the distributions of IL-6 and MAP levels

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          Abstract

          Trier Social Stress Test (TSST) is an experimental psychological test that induces changes in autonomic, endocrinological and immunological activity. Two measures used to evaluate the inflammatory activity induced by this test are the interleukin 6 (IL-6), a cytokine sensitive to changes in sympathetic nervous activity, and the mean arterial pressure (MAP), a measure sensitive to changes in autonomic activity. This study had two goals: first, the study examined whether TSST increases IL-6 and MAP levels; second, pre- and post-TSST IL-6 levels were compared for participants whose IL-6 levels increased or decreased due to the TSST. Saliva samples of IL-6 and MAP were taken from 42 participants clinically healthy, without psychiatric history, and data were analysed via quantile comparisons. The results showed that TSST did not lead to an increase in sympathetic activity as indexed by IL-6. Instead, TSST led to increases in MAP. Also, there were significant differences between the IL-6 distributions of people whose IL-6 levels changed from low to high (63%) and from high to low (37%) before and after the TSST. These findings suggest that the TSST will not have the same effect on all participants; that is, individual differences can be assessed using a biomarker to identify people with specialized psychological care needs.

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          Biological and psychological markers of stress in humans: focus on the Trier Social Stress Test.

          Validated biological and psychological markers of acute stress in humans are an important tool in translational research. The Trier Social Stress Test (TSST), involving public interview and mental arithmetic performance, is among the most popular methods of inducing acute stress in experimental settings, and reliably increases hypothalamic-pituitary-adrenal axis activation. However, although much research has focused on HPA axis activity, the TSST also affects the sympathetic-adrenal-medullary system, the immune system, cardiovascular outputs, gastric function and cognition. We critically assess the utility of different biological and psychological markers, with guidance for future research, and discuss factors which can moderate TSST effects. We outline the effects of the TSST in stress-related disorders, and if these responses can be abrogated by pharmacological and psychological treatments. Modified TSST protocols are discussed, and the TSST is compared to alternative methods of inducing acute stress. Our analysis suggests that multiple readouts are necessary to derive maximum information; this strategy will enhance our understanding of the psychobiology of stress and provide the means to assess novel therapeutic agents. Copyright © 2013 Elsevier Ltd. All rights reserved.
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            Association between plasma IL-6 response to acute stress and early-life adversity in healthy adults.

            Increased production of peripheral cytokines and other pro-inflammatory markers has been linked to psychiatric disorders such as major depressive disorder and post-traumatic stress disorder. Recent research has pointed to early-life stress, particularly childhood maltreatment, as an independent and preventable risk factor for systemic inflammation in adulthood. Some data suggest that adults with a history of childhood maltreatment exhibit a heightened inflammatory response to acute stress challenge. To further elucidate the relationship between childhood maltreatment and pro-inflammatory cytokine production, we examined plasma IL-6 response to the Trier Social Stress Test (TSST) in 69 healthy adult subjects without depression or post-traumatic stress disorder. Serial plasma IL-6 concentrations were measured during a standardized psychosocial stressor in n=19 subjects with moderate-severe childhood maltreatment (MAL), and n=50 controls without maltreatment (CTL), as indicated by self-ratings on the childhood trauma questionnaire (CTQ). CTQ total scores were positively correlated with overall change in IL-6 response, as well as the maximum IL-6 concentration during the TSST. Greater acute IL-6 release and higher IL-6 concentrations over time were observed for the MAL group relative to the CTL group. Inflammation may be an important developmental mediator linking adverse experiences in early life to poor adult physical and mental health. The results of this preliminary study warrant further investigation in a larger sample.
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              Integrating Interleukin-6 into depression diagnosis and treatment

              There is growing evidence of a relationship between inflammation and psychiatric illness. In particular, the cytokine Interleukin-6 (IL-6) has been linked to stress-related disorders such as depression and anxiety. Here we discuss evidence from preclinical and clinical studies examining the role of IL-6 in mood disorders. We focus on the functional role of peripheral and central release of IL-6 on the development of stress susceptibility and depression-associated behavior. By examining the contribution of both peripheral and central IL-6 to manifestations of stress-related symptomatology, we hope to broaden the way the field thinks about diagnosing and treating mood disorders.
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                Author and article information

                Contributors
                Journal
                Heliyon
                Heliyon
                Heliyon
                Elsevier
                2405-8440
                30 April 2019
                April 2019
                30 April 2019
                : 5
                : 4
                : e01580
                Affiliations
                [a ]School of Psychology, National Autonomous University of Mexico, Mexico
                [b ]Interdisciplinary Centre for Health Sciences, National Polytechnic Institute, Mexico
                [c ]Regional Multidisciplinary Research Centre, National Autonomous University of Mexico, Mexico
                [d ]Postgraduate in Mechatronics, Autonomous University of Querétaro, Mexico
                [e ]School of Psychology, The University of Adelaide, Australia
                Author notes
                Article
                S2405-8440(18)39198-9 e01580
                10.1016/j.heliyon.2019.e01580
                6495068
                b0c2854a-03ac-4505-8fb2-f01dfa0ab9b8
                © 2019 Published by Elsevier Ltd.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 29 December 2018
                : 22 March 2019
                : 24 April 2019
                Categories
                Article

                neuroscience,physiology,clinical psychology,psychology
                neuroscience, physiology, clinical psychology, psychology

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