'As above, so below' examining the interplay between emotion and the immune system

Abstract

While the concept of a palpable relationship between our mental and physical well-being is certainly not new, it is only in the light of modern scientific research that we have begun to realize how deeply connected our emotional and immune states may be. We begin this review with a series of studies demonstrating how four fundamental emotional responses: anger, anxiety, mirth and relaxation are able modulate cytokine production and cellular responses to a variety of immune stimuli. These modulations are shown to be either detrimental or beneficial to a patient's health dependent on the context and duration of the emotion. We also discuss the reverse, highlighting research demonstrating how the loss of key immune cells such as T lymphocytes in clinical and animal studies can negatively impact both emotional well-being and cognition. Additionally, to give a more complete picture of the manifold pathways that link emotion and the immune system, we give a brief overview of the influence the digestive system has upon mental and immunological health. Finally, throughout this review we attempt to highlight the therapeutic potential of this burgeoning field of research in both the diagnosis and treatment of immune and disorders. As well as identifying some of the key obstacles the field must address in order to put this potential into practice.

Keywords: autoimmunity; emotion; immunosuppression; inflammation; mental health.

Figure 1

The central nervous system (CNS) mediates the release of various immune influencing glucocorticoids via activation of a series of connected regions within the brain referred to as the hypothalamic–pituitary–adrenal axis. Research suggests the CNS to be primarily immune-suppressive in action, inhibiting production of pro-inflammatory cytokines, chemotactic factors and limiting migration and activation in several immune cell types.– Additionally the CNS elicits differential immune effects dependent on cell type and stage of development, inducing the expansion and migration of immature dendritic cells while seemingly promoting a tolerogenic phenotype in their mature counterparts., Although less studied, several papers have demonstrated that the sympathetic nervous system is able to modulate immune activity through production of epinephrine and norepinephrine promoting a T helper type 2 (Th2) and Th17 phenotype in in T cells and dendritic cells, respectively., Produced by the parasympathetic nervous system, acetylcholine has been shown to interact directly with multiple immune cell subsets through expression of acetylcholine receptors, leading to suppression of a number of pro-inflammatory pathways in macrophages and other immune cells.– Abbreviations: IFN-γ, interferon-γ; IL-17, interleukin-17; NF-κB, nuclear factor-κB; STAT, signal transducer and activator of transcription; Th1, T helper type 1; TNF, tumour necrosis factor.