Repair Activity of Skin Barrier by Chitin-Nanofibrils Complexes

2011 
Stratum Corneum (SC) lipids and corneodesmosomes involved in corneocytes and lamellar packing (1-3), and filaggrin production, responsible of the Normal Moisturizing Factors (NMF) release (4-7), are considered key components of the skin barrier together with the enzymatic antioxidant system (8). SC is composed, in fact, of nucleated keratin-rich corneocytes embedded in a extracellular lipid matrix organized into membrane-like bilayers interconnected by corneodesmosomes (9). Both corneocytes and lipid lamellae, as main component of skin barrier, are responsible for the water retention and diffusion through the skin preventing excess transepidermal water loss (TEWL), while degradation of corneodesmosomes is the key event of the regular shedding and renewing of the SC barrier (10,11). The hallmark of this barrier formation and function lies, in fact, in the intricate balance of epidermal cell differentiation and desquamation events. Nevertheless, while this orchestrated interplay of events can be influenced and perturbed by environmental stressors and ageing, too much damage can enhance epidermal hyperplasia and inflammation (12-14). As a consequence of defects in skin barrier function, mild to severe xerosis appear, which can lead to the penetration of irritants and allergens resulting in immunological and inflammatory processes (15). Atopic Dermatitis (AD) is, for example, a severe xerotic skin disease characterized by a disruption of epidermal barrier function that, increasing the reactivity to common environmental allergens, leads to an allergic-type inflammatory reaction (15-17). According to previous studies (18-20) the disruption of this barrier affecting premature aging also, should be repaired by the use of some antioxidant and immunomodulant compounds complexed with chitin nanofibrils (CN), capable to improve its functionality. The vehicle used results, naturally, of fundamental importance.
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