The effects of psychological stress on humans: Increased production of pro-inflammatory cytokines and a Th1-like response in stress-induced anxiety
ABSTRACT There is some evidence that, in humans and experimental animals, psychological stress may suppress or enhance immune functions, depending on the nature of the stressor and the immune variables under consideration. The possibility that psychological stress may affect the production of pro-inflammatory and immunoregulatory cytokines was investigated in 38 medical students, who had blood samplings a few weeks before and after as well as one day before an academic examination. Psychological stress significantly increased the stimulated production of tumour necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), IL-1 receptor antagonist (IL-1Ra), interferon gamma (IFN-gamma) and IL-10. Students with high stress perception during the stressful condition had a significantly higher production of TNF-alpha, IL-6, IL-1Ra and IFN-gamma than students with a low-stress perception. Students with a high anxiety response had a significantly higher production of IFN-gamma and a lower production of the negative immunoregulatory cytokines, IL-10 and IL-4, than students without anxiety. These findings suggest that, in humans, changes in the production of the pro-inflammatory cytokines, TNF-alpha, IL-6 and IFN-gamma, and negative immunoregulatory cytokines, IL-10 and IL-4, take part in the homeostatic responses to psychological stress and that stress-induced anxiety is related to a T-helper-1-like response.
- SourceAvailable from: Jonathan Godbout
[Show abstract] [Hide abstract]
- "In humans, the experience of chronic stress is associated with proinflammatory leukocytic phenotypes that are unresponsive to the anti-inflammatory actions of glucocorticoids (GCs) (Cohen et al., 2012) and a transcriptional profile that is consistent with the expansion and priming of myeloid-derived cells (Miller et al., 2008; Powell et al., 2013). The mechanistic association between inflammation and depression is particularly well-established (Raison et al., 2006; Dantzer et al., 2008; Miller et al., 2009; Norman et al., 2010; Capuron and Miller, 2011), while the case continues to build for the mechanistic association between inflammation and anxiety (Maes et al., 1998; Pitsavos et al., 2006; O'Donovan et al., 2010; Pace and Heim, 2012). The murine repeated social defeat (RSD) paradigm recapitulates many key immunological and behavioral features associated with psychosocial stress in humans. "
ABSTRACT: The development and exacerbation of depression and anxiety are associated with exposure to repeated psychosocial stress. Stress is known to affect the bidirectional communication between the nervous and immune systems leading to elevated levels of stress mediators including glucocorticoids (GCs) and catecholamines and increased trafficking of proinflammatory immune cells. Animal models, like the repeated social defeat (RSD) paradigm, were developed to explore this connection between stress and affective disorders. RSD induces activation of the sympathetic nervous system (SNS) and hypothalamic-pituitary (HPA) axis activation, increases bone marrow production and egress of primed, GC-insensitive monocytes, and stimulates the trafficking of these cells to tissues including the spleen, lung, and brain. Recently, the observation that these monocytes have the ability to traffic to the brain perivascular spaces and parenchyma have provided mechanisms by which these peripheral cells may contribute to the prolonged anxiety-like behavior associated with RSD. The data that have been amassed from the RSD paradigm and others recapitulate many of the behavioral and immunological phenotypes associated with human anxiety disorders and may serve to elucidate potential avenues of treatment for these disorders. Here, we will discuss novel and key data that will present an overview of the neuroendocrine, immunological and behavioral responses to social stressors. Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.Neuroscience 01/2015; 289. DOI:10.1016/j.neuroscience.2015.01.001 · 3.33 Impact Factor
[Show abstract] [Hide abstract]
- "Positive correlation between scores from STAI and PSQ were also observed in other study (Bergdahl & Bergdahl, 2002). Since anxiety can induce the stress (Maes et al., 1998), the correlation between these scores was also expected. High anxiety levels and high stress can lead to: immunity depression (Cohen, Tyrrell, & Smith, 1991); increased days of missed work (Pflanz & Ogle, 2006) and; psychiatric, metabolic and autoimmune diseases (Kumar, Rinwa, Kaur, & Machawal, 2013). "
ABSTRACT: The objectives of this study were: 1) identify the state anxiety, trait anxiety levels and perceived stress levels of food handlers and; 2) Verify the association of these scores with food safety variables like: food safety knowledge, attitudes, practices and with job characteristics. This study involved 183 randomly selected food handlers from different food businesses in Santos city, Brazil, as follows: street food kiosks, beach kiosks, restaurants, hospitals and school meal services. To evaluate knowledge, attitudes and self-reported practices, a structured questionnaire was used. Observed practices were evaluated using a checklist. The State Trait Anxiety Inventory – STAI was applied to assess the levels of state and trait anxiety with a score range from 10 to 80. To evaluate stress the Perceived Stress Questionnaire – PSQ was used with a score range from zero to one. Food handlers presented 39.22; 10.1 (mean; standard deviation) of state anxiety score, 39.58; 9.6 of trait anxiety score and a perceived stress score of 0.36; 0.09. Observed practices presented a weak negative correlation with state anxiety (r = −0.26; p = 0.014) but not with trait anxiety (r = −0.18; p = 0.09) and stress (r = 0.03; p = 0.78). Using generalized linear models were observed that a higher stress level, trait anxiety and state anxiety were found in food handlers who do not participated in food safety training and with lower knowledge scores of food safety. These findings show that training can not only improve knowledge but possibly empower food handlers, increase their self-efficacy and reduce anxiety and stress levels.Food Control 10/2014; 50:684–689. DOI:10.1016/j.foodcont.2014.10.012 · 2.82 Impact Factor
[Show abstract] [Hide abstract]
- "Stress and anxiety are behaviorally as well as biologically linked in both humans and rodents  . In mice, anxiety-like behaviors can be assessed by examining behavioral change in the open field test, the social interaction test, and the marble-burying test [20–25,37–40]. "
ABSTRACT: Psychological stress can have devastating and lasting effects on a variety of behaviors, especially those associated with mental illnesses such as anxiety and depression. Animal models of chronic stress are frequently used to elucidate the mechanisms underlying the relationship between stress and mental health disorders and to develop improved treatment options. The current study expands upon a novel chronic stress paradigm for mice: predatory stress. The predatory stress model incorporates the natural predator-prey relationship that exists among rats and mice and allows for greater interaction between the animals, in turn increasing the extent of the stressful experience. In this study, we evaluated the behavioral effects of exposure to 15 days of predatory stress on an array of behavioral indices. Up to 2 weeks after the end of stress, adult male mice showed an increase of anxiety-like behaviors as measured by the open field and social interaction tests. Animals also expressed an increase in depressive-like behavior in the sucrose preference test. Notably, performance on the novel object recognition task, a memory test, improved after predatory stress. Taken as a whole, our results indicate that 15 exposures to this innovative predatory stress paradigm are sufficient to elicit robust anxiety-like behaviors with evidence of co-morbid depressive-like behavior, as well as changes in cognitive behavior in male mice.Behavioural Brain Research 09/2014; 275. DOI:10.1016/j.bbr.2014.08.060 · 3.39 Impact Factor