Regulation of cutaneous immunity by catecholamines

Abstract

The Sympathetic Nervous System and Stress Responses: An activation of the sympathetic nervous system (SNS), one of the main pathways involved in the stress response, produces an immediate, widespread fight or flight response. Transmitters of the SNS triggered during stress also shape the general and the cutaneous immune response. Catecholamines: The catecholamines epinephrine and norepinephrine act as hormones in the blood circulation and as neurotransmitters in the central and peripheral nervous system. Catecholamine (or adrenergic) receptors are abundantly expressed on resident and infiltrating skin cells. Cutaneous Immunity: Cutaneous immune function is regulated by multiple neuroendocrine pathways, among them are the hypothalamic pituitary axis, glucocorticoids, neuropeptides, endogenous opioids, and, prominently, the SNS. Langerhans cells in the skin have been shown to respond to adrenergic signals by altering their ability to present antigens, produce cytokines, express co-stimulatory molecules and migrate to draining lymph nodes. Atopic Dermatitis: Flares of atopic dermatitis are often reported to be triggered by stressful life events, and a dysregulation of the adrenergic response has been linked to immunological abnormalities. The relevance of psychosocial stress as a trigger factor is emphasized by the therapeutic effect of psychosocial interventions. Psoriasis: β-Adrenergic receptor blocking drugs can induce the first manifestation or exacerbation of psoriasis. Catecholamines suppress Th1 responses and skew the immune response towards Th2 through β-adrenergic receptors. The pharmacologic blockade of β-receptors may, thus, lead to a predominance of Th1 pathways and initiation or exacerbation of disease in genetically predisposed individuals. © 2009 Springer Berlin Heidelberg.