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Peters E.M.J.,Charite - Medical University of Berlin | Peters E.M.J.,Justus Liebig University | Michenko A.,Charite - Medical University of Berlin | Michenko A.,Justus Liebig University | And 7 more authors.
PLoS ONE | Year: 2014

Rationale: 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). Methods: 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. Results: 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. Conclusions: 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. © 2014 Peters et al. Source


Sobolev V.V.,Russian Academy of Sciences | Piruzyan A.L.,Russian Academy of Sciences | Minnibaev M.T.,chenov Moscow Medical University | Sautin M.E.,Russian Academy of Sciences | Bruskin S.A.,Russian Academy of Sciences
Bulletin of Experimental Biology and Medicine | Year: 2011

Expression of ATF-3 and ATF-4 genes was examined quantitatively by real-time PCR and changes in the expression of these genes in atherosclerotic lesions and in psoriatic skin were demonstrated. It was found that concomitant pathologies do not affect the expression of these genes. Opposite changes in the expression of ATF-3 and ATF-4 genes in atherosclerotic and psoriatic samples were revealed and a hypothesis was put forward that this parameter could be a criterion of pathological process in both diseases. © 2011 Springer Science+Business Media, Inc. Source


Sapin M.R.,chenov Moscow Medical University | Aminova G.G.,Russian Academy of Medical Sciences | Shvetsov E.V.,chenov Moscow Medical University | Salim A.R.,chenov Moscow Medical University | Chetvertkov V.S.,chenov Moscow Medical University
Bulletin of Experimental Biology and Medicine | Year: 2011

The structure of gastric wall was studied by histological methods in Wistar rats in health and after skull trephination and insertion of a needle into the brain. Experimental brain injury led to the development of destructive changes in the gastric wall (in the lymphoid structures located between the gland bottoms and muscle plate of the mucosa). Changes in the structure of cardiac glands and desquamation of the epithelium were detected. Microcirculation was disordered, signs of infl ammation appeared. The counts of medium-sized lymphocytes and plasma cells increased in the layer of lymphoid cells and in the submucosa. © 2011 Springer Science+Business Media, Inc. Source

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