Measurement of trihydroxy-linoleic acids in stratum corneum by tape-stripping: Possible biomarker of barrier function in atopic dermatitis

Abstract

Epidermal ceramides are indispensable lipids that maintain the functions of the stratum corneum. Esterified omega-hydroxyacyl-sphingosine (EOS) ceramide with a linoleate moiety is one of the most important ceramide species for forming cornified lipid envelopes. This linoleate moiety is eventually metabolized to trihydroxy-linoleic acid (triol, 9,10,13-trihydroxy-11E-octadecenoic acid). Thus, we assumed that a decrease of triols might reflect skin barrier dysfunction. Against this background, the purposes of this study were to measure the triols by a simple tape-stripping method and to determine the correlation between the amount of triols and transepidermal water loss (TEWL) as an indicator of barrier dysfunction in atopic dermatitis patients. Twenty Japanese subjects with normal skin and 20 atopic dermatitis patients were enrolled in this study. TEWL was measured and triols of the stratum corneum were analyzed by tape-stripping. The results showed for the first time that triols in the stratum corneum could be simply measured using the tape-stripping method. The triol levels in atopic dermatitis patients were much higher than those in healthy subjects. Moreover, the triol levels correlated with TEWL of non-lesional forearm skin in patients with atopic dermatitis. The results suggest that the assaying of triol levels via non-invasive tape-stripping could be beneficial for monitoring barrier function in atopic dermatitis.

SDR9C7 catalyzes critical dehydrogenation of acylceramides for skin barrier formation

“…The HPLC analysis used an Agilent 1200 series system with an Agilent Eclipse XBD-C18 column (5 μm, 15 × 0.46 cm), a solvent of acetonitrile/water/glacial acetic acid (75/25/0.01 by volume) at a flow rate of 1 mL/min, with the diode array detector set to monitor at 205, 220, 235, and 270 nm. a biomarker of barrier function (8). According to our new concept, there is no requirement for the unidentified missing esterase (5,13) to remove the oxidized linoleate and provide free CerOS for coupling to protein.…”

“…Defects in genes involved in biosynthesis of CerEOS or its processing to form the CLE result in the severe skin disorder autosomal recessive congenital ichthyosis (ARCI), characterized by dry skin, scaling, hyperkeratosis, and occasional erythroderma (6,7). Moreover, alterations of epidermal lipid homeostasis, especially contents of CerEOS and other ceramides, are linked to atopic dermatitis (8). Thus, abnormal metabolism of epidermal ceramides underlies the pathogenesis of various skin diseases associated with defective skin barrier function.…”

The IL‐13–OVOL1–FLG axis in atopic dermatitis

“…Skin barrier function is disrupted in AD compared with that in normal controls . The epidermal barrier is formed by the coordinated and sequential cross‐linking of epidermal differentiation molecules such as FLG and intercellular lipids and corneocyte adhesion .…”

“…Skin barrier function is disrupted in AD compared with that in normal controls. [47][48][49] The epidermal barrier is formed by the coordinated and sequential cross-linking of epidermal differentiation molecules such as FLG and intercellular lipids and corneocyte adhesion. [47][48][49] The expression of FLG and the other differentiation molecules loricrin and involucrin is down-regulated or expressed prematurely in the lesional and non-lesional skin of AD compared with their expression in the normal skin of healthy individuals.…”

“…[47][48][49] The epidermal barrier is formed by the coordinated and sequential cross-linking of epidermal differentiation molecules such as FLG and intercellular lipids and corneocyte adhesion. [47][48][49] The expression of FLG and the other differentiation molecules loricrin and involucrin is down-regulated or expressed prematurely in the lesional and non-lesional skin of AD compared with their expression in the normal skin of healthy individuals. 7,50,51 As the daily application of moisturizer during the first 32 weeks of life reduces the risk of AD in infants, 52 skin barrier dysfunction is essential to the development of AD.…”