Yanxia Lu,1,2* Tze Pin Ng,3 Anis Larbi2,4
Proceedings of the Nature Research Society, Volume 2, Article Number 02005, 2018
Published Online: 28 May 2018 (Review)
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The prevalence of asthma morbidity and mortality has increased significantly in recent decades, concurrently with increasing mental health problems worldwide. Asthma has long been considered as an archetypal psychosomatic disease. However, evidence supporting the link between psychosocial stress and asthma is just emerging. The stress-asthma link is supported by evidence that chronic stress suppresses hypothalamo-pituitary-adrenocortical (HPA) axis activity and its anti-inflammatory effect, resulting in blunted HPA axis responsiveness seen in asthma patients. However, marked inter-individual variability in responses to stress exists. Some are more vulnerable than others to the effects of stress in terms of asthma risks and morbidity. Recent studies suggest the main contribution of neuropeptide Y (NPY) in modulating HPA-axis responsiveness and explaining inter-individual variation in resilience to stress and asthma in animal models and clinical samples. The temporal and spatial expression pattern of NPY and its receptors (Y1 and Y5) is determined in the airways of asthmatic mice. Peripheral NPY concentration and the genetic variation in the NPY gene has been investigated in asthma in multiple studies. Studies have attempted to explain the underlying mechanisms of the "neuroimmune" crosstalk as a contributor to the development of the airway inflammation and asthma. Such a psychoneuro-immunological perspective in asthma research represents a new psychosomatic approach in pharmacological therapy of asthma, and may open the door for future potential use of NPY agonists in treating asthma. Future brain imaging research using specific NPY-receptor ligands is required to better understand the relationship between central release of NPY and asthma.