Purpose of review: Biological hypersensitivity to environmental stimuli is a fundamental feature of atopy predisposing to a number of clinically expressed disorders including allergic rhinitis, atopic dermatitis or eczema, and allergic asthma. There is provocative evidence that psychological stress constitutes an increased risk for atopy. This risk is thought to be mediated by the effects of stress on neuroimmunoregulation which in turn modulates the hypersensitivity response. The primary objective is to review recent evidence updating our understanding of the role for psychological stress in atopy.
Recent findings: The Th1-Th2 paradigm has been central to interpreting quantitative differences in cytokine expression in response to environmental stimuli like stress. Here we argue that examination of other mechanisms (e.g. oxidative stress pathways, glucocorticoid resistance, nerve-mast cell interactions, intestinal dysbiosis) and a broader range of cytokines and neuropeptides produced by cells both within and outside the immune system may better delineate the true complexity of the underlying mechanisms linking stress to allergic sensitization and asthma. The role of genetics and gene by environment interactions - based on evolving knowledge of candidate genes that may be relevant to both the stress response in general and pathways linked specifically to atopy - is also discussed.
Summary: Psychological stress may be conceptualized as a social pollutant that, when 'breathed' into the body, may disrupt biological systems related to inflammation through mechanisms potentially overlapping with those altered by physical pollutants and toxicants.
Abbreviations HPA: hypothalamic-pituitary-adrenocortical; SAM: sympathetic and adrenomedullary; TNF: tumor necrosis factor.