Stress and inflammation in exacerbations of asthma

University of British Columbia, Department of Psychology, 2136 West Mall, Vancouver, BC, Canada V6T 1Z4.
Brain Behavior and Immunity (Impact Factor: 5.89). 12/2007; 21(8):993-9. DOI: 10.1016/j.bbi.2007.03.009
Source: PubMed


In this mini-review, we outline a model depicting the immunologic mechanisms by which psychological stress can exacerbate clinical symptoms in patients with asthma. This model highlights the importance of both social and physical exposures in the exacerbation of asthma symptoms. The basic premise of the model is that psychological stress operates by altering the magnitude of the airway inflammatory response that irritants, allergens, and infections bring about in persons with asthma. The biological pathways for how stress amplifies the immune response to asthma triggers include the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic-adrenal-medullary (SAM) axis, and the sympathetic (SNS) and parasympathetic (PNS) arms of the autonomic nervous system. Empirical evidence for this model is reviewed, and conclusions and future research directions are discussed.

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    • "In addition, the hypothalamus also activates the adrenal medulla via the sympathetic nervous system (SNS), resulting in the release of the catecholamines adrenalin and noradrenalin. ACTH, CRH and glucocorticoids (GCs) in turn provide negative feedback to dampen and cease the signaling cascade and return to homeostasis (Meijer, 2006; Chen and Miller, 2007). In addition, activation of the autonomic nervous system, both centrally and via afferent pathways, activates efferent neuronal circuits, including the cholinergic anti-inflammatory reflex (Tracey, 2009). "
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    ABSTRACT: Cardiovascular disease (CVD) remains a leading cause of death worldwide and identification and therapeutic modulation of all its risk factors is necessary to ensure a lower burden on the patient and on society. The physiological response to acute and chronic stress exposure has long been recognized as a potent modulator of immune, endocrine and metabolic pathways, however its direct implications for cardiovascular disease development, progression and as a therapeutic target are not completely understood. More and more attention is given to the bidirectional interaction between psychological and physical health in relation to cardiovascular disease. With atherosclerosis being a chronic disease starting already at an early age the contribution of adverse early life events in affecting adult health risk behavior, health status and disease development is receiving increased attention. In addition, experimental research into the biological pathways involved in stress-induced cardiovascular complications show important roles for metabolic and immunologic maladaptation, resulting in increased disease development and progression. Here we provide a concise overview of human and experimental animal data linking chronic and acute stress to CVD risk and increased progression of the underlying disease atherosclerosis. Copyright © 2015. Published by Elsevier Inc.
    No preview · Article · Aug 2015 · Brain Behavior and Immunity
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    • "In experimental studies, stress has been shown to accentuate the airway inflammatory response to irritants, allergens, and infections and, in doing so, increases the frequency, duration, and severity of the person's symptoms (Chen, 2007). How stress affects asthma is relatively well documented (Gibson, 2010), while sound prospective studies on the relationship between stress and incidence of asthma and other atopic disorders such as rhinitis and dermatitis are still few and the results are conflicting. "
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    ABSTRACT: Objective: This study aimed to investigate the prediction of asthma control on the basis of perceived stress, locus of control, and self-efficacy in adult patients with asthma. Methods: This was a descriptive-correlative and cross-sectional study.The solecty of this study is all asthmatic patients in Tehran. our sample consisted of 100 participants who were selected by purposeful sampling method. A total of 100 patients with asthma were selected among outpatients of Masih Daneshvari Hospital. Participants included 52 women and 48 men. Their mean (±SD) age was 36.12 (±9.82) years. Sociodemographic data were collected and Perceived Stress Scale (PSS), Multidimensional Health Locus of Control (MHLC), Asthma Self-efficacy Scale (ASES), and Asthma Control Test (ACT) were applied. Data were analyzed by Pearson correlation and multiple regression analysis. Statistical analysis was performed using the SPSS ver. 16.0. Results: The results indicated that there were negative significant relationships between perceived stress, dimension of external control (chance) and asthma control, but positive significant relationships between self-efficacy and asthma control. In regression analysis, the perceived stress was the predictor of asthma control. Conclusion: In this study, our findings suggest that perceived stress has an important role in the development and maintenance of asthma symptoms. In addition, self-efficacy and a tendency to externally attribute the locus of control (chance) are significantly associated with asthma control.
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    • ", 2010 , 2013 ) , with some data suggesting that such effects persist despite subsequent improvements in the surrounding environment ( G . Miller & Chen , 2007 ) . One possibility , therefore , is that early life stress increases lifetime risk for depression and depression - related disease conditions in part by heightening an individual ' s sensitivity to stress , which in turn drives the emer - gence of an increasingly proinflammatory phenotype ( see G . "
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    ABSTRACT: Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
    Full-text · Article · Jan 2014 · Psychological Bulletin
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