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: 6.13). 12/2007; 21(8):993-9. DOI: 10.1016/j.bbi.2007.03.009
Source: PubMed

ABSTRACT 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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    • ", 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).
    Psychological Bulletin 01/2014; 140(3). DOI:10.1037/a0035302 · 14.39 Impact Factor
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    • "So, once a person catches cold or flu, stress can exacerbate symptoms (Chen and Miller, 2007; Qureshi et al., 2002). "
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    ABSTRACT: Stress in health sciences students has been studied extensively. Nevertheless, only few studies have been conducted on pharmacy students and nothing was done to compare stress effects on the immune responses of Pharmacy and Doctor of Pharmacy (PharmD) students. The aim of this pilot study was (1) to measure the self-reported perceived stresses, immune-related diseases and health outcomes of pharmacy and PharmD students, (2) to investigate the relationship between perceived stresses, health outcomes and immune-related diseases and (3) to compare stress induced changes in the health and immune system of pharmacy and PharmD students. The study represents a cross sectional survey using an interviewer administered questionnaire about stress and students' health states during the fall semester of 2009/2010. At commence of this study, 222 of pharmacy and PharmD participant students (113 and 109 respectively) from the third and uppermost levels of study were picked up randomly. They were found to perceive stress related to program intensity, lack of exercise and social activities, bad nutritional routines and accommodation. Effects of increased study loads on students' health and immune-related diseases were more pronounced on PharmD students, while showing significant changes on Pharmacy students. In general, more than 50% of students of each program got ill several times, mainly during the midterm period, had cold/flu, were under medical care and had problems in skin and/or hair. Also, PharmD students reported relatively higher levels of perceived stress and lower emotional and satisfaction quality of life compared to Pharmacy students. Results may help to increase the awareness of students to get prepared to what they might face, and may enable them to reduce the program's negative effects.
    Saudi Pharmaceutical Journal 01/2013; 21(1):35-44. DOI:10.1016/j.jsps.2012.02.006 · 1.00 Impact Factor
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    • "Airways were narrowed and goblet cell hyperplasia was evident, both known features of asthma pathogenesis. These results are consistent with clinical findings that link stress and pulmonary airway disease among asthmatics (Chen, Miller 2007). "
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    ABSTRACT: Epidemiological and experimental studies suggest a positive correlation between chronic respiratory inflammatory disease and the ability to cope with adverse stress. Interactions between neuroendocrine and immune systems are believed to provide insight toward the biological mechanisms of action. The utility of an experimental murine model was employed to investigate the immunological consequences of stress-controllability and ovalbumin-induced airway inflammation. Pre-conditioned uncontrollable stress exacerbated OVA-induced lung histopathological changes that were typical of Th2-predominant inflammatory response along respiratory tissues. Importantly, mice given the ability to exert control over aversive stress attenuated inflammatory responses and reduced lung pathology. This model represents a means of investigating the neuro-immune axis in defining mechanisms of stress and respiratory disease.
    Journal of neuroimmunology 05/2010; 225(1-2):13-21. DOI:10.1016/j.jneuroim.2010.03.010 · 2.79 Impact Factor
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