Psychological Stress can Trigger Atopic Dermatitis in NC/Nga Mice: An Inhibitory Effect of Corticotropin-Releasing Factor

Abstract

Atopic dermatitis (AD) is one of the most common inflammatory diseases of the skin and is usually associated with a family history of atopic diathesis. It has been well established that many environmental or psychological factors aggravate AD. However, it is not clear whether psychological stress by itself can trigger AD. We examined the effect of psychological stress on the onset of AD, using an animal model, the NC/Nga mouse. The animals were exposed to the water avoidance stress (WAS) test to induce psychological stress. Additionally, we examined how corticotropin-releasing factor (CRF) affected the development of AD induced by psychological stress. Under specific pathogen-free (SPF) conditions, NC/Nga mice did not develop AD-like skin lesions. In contrast, NC/Nga mice exposed to psychological stress developed AD-like skin lesions along with elevated levels of serum immunoglobulin E even when kept under SPF conditions. The AD-like skin lesions induced by WAS were completely blocked by pretreating the animals with CRF. Our data indicate that a psychological factor is capable of eliciting AD-like skin lesions in NC/Nga mice. It is possible that the inhibitory effect of CRF may be mediated by the functional modification of various cells that have CRF receptors.

Hypothalamus–pituitary–adrenal axis daily fluctuation, anxiety and age interact to predict cortisol concentrations in boys with an autism spectrum disorder

“…Hypercortisolaemia has also been shown to cause atopic dermatitis [24] and suppressed skin immunity [25]. Other outcomes of excessively high levels of cortisol expression include decreased immunocompetence [26], increased risk of infection, osteoporosis, steroid diabetes, and destruction of hippocampal neurons leading to cell loss, depression and chronic distress [25,27].…”

The Non-Neuronal Cholinergic System in Health and Disease

“…Allergens, infections, environmental pollutants and emotional stress trigger the clinical onset of disease with main features being eczematous skin lesions [25]. In a mouse model the histopathology of atopic dermatitis could be completely prevented by pretreatment with corticotropin-releasing hormone which is released in response to cholinergic stimulation [26]. These results indicate that ACh and the cholinergic system are involved in the regulation of atopic dermatitis [27].…”

Neurobiological Pathways between Chronic Stress and Depression: Dysregulated Adaptive Mechanisms?

“…36 Prolonged and elevated expression of cortisol leads to increased serum lipids, endothelial damage and resultant incidence of coronary heart disease (CHD) [50][51][52] and acute respiratory failure. 46 Hypercortisolaemia has also been shown to cause atopic dermatitis 53 and suppressed skin immunity. 11,54 Other outcomes of excessively high levels of cortisol expression include decreased immunocompetence, 55,56 increased risk of infection, osteoporosis, steroid diabetes, and destruction of hippocampal neurons leading to cell loss, depression and chronic distress.…”