Article

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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    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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