ABSTRACT
Emollients are commonly used for their effectiveness on atopic skin, supported by a few clinical studies suggesting their potential role as corticosteroid sparing agents. We investigated the effect of a new natural emollient on corticosteroid sparing and quality of life of young atopic children and their family. Eighty-six patients (4-48 mos) with moderate atopic dermatitis were randomized by 20 pediatricians to five groups for 21 days: corticosteroids (from twice daily to one application every other day) combined or not with the studied cream (twice daily), and evaluated by SCORAD and specific quality of life questionnaires. At the end of the study, all five groups were statistically improved in terms of SCORAD and quality of life index. Thus, application of a topical corticosteroid every other day in addition to the studied cream was as effective as a once or twice daily application of the steroid alone. The studied cream had a significant impact on lichenification, excoriation and quality of life. A twice daily application of a new natural emollient provided a major corticosteroid sparing, improved lichenification and excoriation and improved the quality of life in children and their parents.
Subject(s)
Adrenal Cortex Hormones/administration & dosage , Dermatitis, Atopic/drug therapy , Dermatitis, Atopic/physiopathology , Emollients/therapeutic use , Plant Oils/chemistry , Quality of Life , Administration, Topical , Child, Preschool , Drug Administration Schedule , Drug Therapy, Combination , Emollients/chemistry , Female , Humans , Infant , Male , Parents , Severity of Illness Index , Sunflower Oil , Surveys and QuestionnairesABSTRACT
Matrix metalloproteinase (MMP)-2 and MMP-9 are involved in keratinocyte migration and granulation tissue remodeling during wound healing. Thermal water cures are sometimes proposed as complementary treatment for accelerating healing of wounds resulting from burns and/or surgery, but their mechanisms of action remain unknown. Some thermal waters are rich in trace elements such as boron and manganese. Interestingly, clinical studies have shown the beneficial effects of trace elements such as boron and manganese for human wound healing. To try to specify the role of trace elements in cutaneous healing, the present study investigated the effects of these trace elements on the production of MMP-2 and MMP-9 by normal human keratinocytes cultured in vitro. Immunohistochemistry and Western blot showed that intracellular MMP-9 expression in keratinocytes was induced when incubated for 6 h with boron at 10 micro g/ml or manganese at 0.2 micro g/ml. Moreover, gelatin zymography on keratinocyte supernatants showed an increase of gelatinase secretion after 24 h of incubation of keratinocytes with boron or manganese, regardless of concentration. Gelatinase secretion was not associated with keratinocyte proliferation induced by trace elements. Thus, our results suggest that boron and manganese could play a role in the clinical efficiency of thermal water on wound healing.
Subject(s)
Boron/metabolism , Hydrotherapy/methods , Keratinocytes/enzymology , Manganese/metabolism , Matrix Metalloproteinase 2/biosynthesis , Matrix Metalloproteinase 9/biosynthesis , Blotting, Western , Cell Proliferation , Cells, Cultured , Dose-Response Relationship, Drug , Hot Temperature , Humans , Immunoblotting , Immunohistochemistry , In Vitro Techniques , Keratinocytes/cytology , Keratinocytes/metabolism , RNA, Messenger/metabolism , Skin/metabolism , Time Factors , Trace ElementsABSTRACT
Keratinocyte proliferation and migration are essential for the reconstruction of the cutaneous barrier after skin injury. Interestingly, thermal waters which are rich in trace elements (e.g. boron and manganese), are known to be able to improve wound healing. In order to understand the mechanism of action of this effect, our study investigated the in vitro modulation of keratinocyte migration and proliferation by boron and manganese salts, which are present in high concentrations in a thermal water (Saint Gervais). Our in vitro study demonstrated that incubating keratinocytes for 24 h with boron salts at concentrations between 0.5 and 10 microg/ml or manganese salts at concentrations between 0.1 and 1.5 microg/ml accelerated wound closure compared with control medium (+20%). As this acceleration was not related to an increase in keratinocyte proliferation we suggest that boron and manganese act on wound healing mainly by increasing the migration of keratinocytes.
Subject(s)
Boron/pharmacology , Cell Movement/drug effects , Keratinocytes/metabolism , Manganese/pharmacology , Cells, Cultured , Humans , Keratinocytes/cytology , Wound Healing/drug effects , Wound Healing/physiologyABSTRACT
BACKGROUND: Interferon-alpha and -gamma are glycoproteins with antiviral and immunoregulatory properties. In vitro studies have shown a role for these cytokines in the regulation of epidermal keratinocyte growth and differentiation. In the same way, integrins are adhesion molecules which regulate keratinocyte proliferation and differentiation. AIM: To determine whether the regulatory activity of interferons on keratinocyte proliferation and differentiation is related to a modulation of keratinocyte integrins. METHODS: Two different methods were used: monolayers and reconstituted skin, incubated either with 1,200 U/mL interferon-alpha or 500 U/mL interferon-gamma or control medium for 48 h. The integrin expression was assessed by flow cytometry and immunohistochemistry. RESULTS: In monolayers, only the alpha3 subunit was significantly inhibited by interferon-gamma. In reconstituted skin, where keratinocytes are differentiated, both interferons had an inductive effect on beta1 expression and interferon-alpha had an inhibitory effect on alpha6 expression. CONCLUSION: Interferon-alpha and -gamma induce a modulatory effect on alpha3, alpha6 and beta1 which appears to be related to the state of differentiation. Moreover, the decreased expression of alpha6 and alpha3 could be one of the mechanisms involved in the formation of bullous lesions during long-term interferon therapy.
