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Neurodermitis Und Stress

A. V. Mitschenko, A. N. Lwow, J. Kupfer, V. Niemeier, U. Gieler
Published 2008 · Medicine

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ZusammenfassungEs wird allgemein angenommen, dass Stress einen Einfluss auf die Entstehung oder zumindest Verschlimmerung der Neurodermitis hat. Die psychoimmunologischen Mechanismen, wie sich durch Stress eine Hautentzündung entwickelt, sind bisher nicht ganz klar. Dieses Thema wurde jedoch in den letzten Jahren intensiv erforscht, und die Studien beschäftigen sich mit verschiedenen Erklärungsaspekten: Neuroimmunologische, psychoendokrinologische Studien und Untersuchungen zur Integrität und Funktion der Hautbarriere bei Stress. Verschiedene Neuropeptide und Neurotrophine scheinen eine wichtige Rolle bei stressinduzierten neurogenen Entzündungsprozessen und der Verbindung von Nerven- und Immunsystem zu einzunehmen. Mastzellen spielen dabei eine Schlüsselrolle in der Entwicklung von entzündlichen Reaktionen infolge von Stress. Die Hautbarriere wird unter Stressbedingungen durch Steigerung des Kortisolspiegels zerstört. Dabei ist die Bildung von Lamellarkörperchen vermindert und die epidermale Expression von antimikrobiellen Peptiden (β-Defensin und Cathelicidin) gehemmt. In diesem Beitrag wird eine Übersicht über die aktuellen Forschungsaspekte gegeben.AbstractIt is widely accepted, that stress can induce or exacerbate atopic dermatitis. The physiological mechanisms that mediate this negative influence of stress on atopic dermatitis are not clearly understood. This topic has been actively investigated in recent years focusing on neuroimmunological, psychoendocrinological studies and examination of integrity and function of skin barrier under stress. Different neuropeptides and neurotrophins seem to play an important role in stress-induced neurogenic inflammation and connection of nervous and immune system. Mast cells play a key role in the development of inflammatory reaction to stress. Skin barrier is altered by stress by means of increased cortisol level. Thereby lamellar body secretion is decreased and epidermal expression of antimicrobial peptides (β-defensin and cathelicidin) is down-regulated. We review recent investigations in this field.
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