Mental stress in atopic dermatitis--neuronal plasticity and the cholinergic system are affected in atopic dermatitis and in response to acute experimental mental stress in a randomized controlled pilot study

In mouse models for atopic dermatitis (AD) hypothalamus pituitary adrenal axis (HPA) dysfunction and neuropeptide-dependent neurogenic inflammation explain stress-aggravated flares to some extent. Lately, cholinergic signaling has emerged as a link between innate and adaptive immunity as well as str...

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Published in:PloS one 2014-12, Vol.9 (12), p.e113552-e113552
Main Authors: Peters, Eva Milena Johanne, Michenko, Anna, Kupfer, Jörg, Kummer, Wolfgang, Wiegand, Silke, Niemeier, Volker, Potekaev, Nikolay, Lvov, Andrey, Gieler, Uwe
Format: Article
Language:English
Subjects:
Adaptive immunity
Adolescent
Adult
Analysis
Animal models
Animals
Antigens, Ly - biosynthesis
Antigens, Ly - metabolism
Atopic dermatitis
Biology and Life Sciences
Biopsy
Cell activation
Cholinergic transmission
Correlation analysis
Cytokines
Dermatitis
Dermatitis, Atopic - complications
Dermatitis, Atopic - metabolism
Dermatitis, Atopic - physiopathology
Dermatology
Eczema
Ethics
Growth factors
Humans
Hypothalamus
Immunity
Immunity, Innate
Inflammation
Inflammation - immunology
Inflammation - metabolism
Inflammation - physiopathology
Inflammatory diseases
Internal medicine
Laboratories
Ly-6 antigen
Mast cells
Mast Cells - metabolism
Mast Cells - pathology
Medical treatment
Medicine
Mice
Middle Aged
mRNA
Nerve Fibers - metabolism
Nerve Fibers - pathology
Nerve growth factor
Neural plasticity
Neuronal Plasticity - immunology
Neurons
Pituitary
Plasticity (neural)
Polymerase chain reaction
Proteins
Psychological stress
Psychosomatic medicine
Receptors
Receptors, Nicotinic - biosynthesis
Receptors, Nicotinic - metabolism
RNA
Rodents
Skin
Skin diseases
Social interactions
Stress (Psychology)
Stress, Psychological - complications
Stress, Psychological - immunology
Stress, Psychological - metabolism
Stress, Psychological - physiopathology
Studies
U-Plasminogen activator
Urokinase
Urokinase-Type Plasminogen Activator - biosynthesis
Urokinase-Type Plasminogen Activator - metabolism
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Summary:In mouse models for atopic dermatitis (AD) hypothalamus pituitary adrenal axis (HPA) dysfunction and neuropeptide-dependent neurogenic inflammation explain stress-aggravated flares to some extent. Lately, cholinergic signaling has emerged as a link between innate and adaptive immunity as well as stress responses in chronic inflammatory diseases. Here we aim to determine in humans the impact of acute stress on neuro-immune interaction as well as on the non-neuronal cholinergic system (NNCS). Skin biopsies were obtained from 22 individuals (AD patients and matched healthy control subjects) before and after the Trier social stress test (TSST). To assess neuro-immune interaction, nerve fiber (NF)-density, NF-mast cell contacts and mast cell activation were determined by immunohistomorphometry. To evaluate NNCS effects, expression of secreted mammal Ly-6/urokinase-type plasminogen activator receptor-related protein (SLURP) 1 and 2 (endogenous nicotinic acetylcholine receptor ligands) and their main corresponding receptors were assessed by quantitative RT-PCR. With respect to neuro-immune interaction we found higher numbers of NGF+ dermal NF in lesional compared to non-lesional AD but lower numbers of Gap43+ growing NF at baseline. Mast cell-NF contacts correlated with SCORAD and itch in lesional skin. With respect to the NNCS, nicotinic acetylcholine receptor α7 (α7nAChR) mRNA was significantly lower in lesional AD skin at baseline. After TSST, PGP 9.5+ NF numbers dropped in lesional AD as did their contacts with mast cells. NGF+ NF now correlated with SCORAD and mast cell-NF contacts with itch in non-lesional skin. At the same time, SLURP-2 levels increased in lesional AD skin. In humans chronic inflammatory and highly acute psycho-emotional stress interact to modulate cutaneous neuro-immune communication and NNCS marker expression. These findings may have consequences for understanding and treatment of chronic inflammatory diseases in the future.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0113552