Oleic Acid 도포에 의한 Hairless mouse의 피부투과장벽 및 표피의 변화

최응호,안성구,이승헌 ( Eung Ho Choi,Sung Ku Ahn,Seung Hun Lee ) 대한피부과학회 1997 대한피부과학회지 Vol.35 No.4

Background: The stratum corneum(SC) inhibits t,ransepidermal water loss and makes a permeability barrier against foreign materials, so strategies to overcome relative impermeability of the SC is very important in transdermal drug delivery. This includes occlusion, hydration, chemical permeation enhancers, iontophoresis and sonophoresis, Oleic acid, which is one of the cis-unsaturated fatty acid and chemical permeation enhancers, increases the permeability of the lipophilic molecules and polar miolecules through the SC. By spectrometry, calorimetry and the flux technique, the hypothesis that oleic acid does exist as a liquid within the SC lipids and enhances the transport of polar molecules across the SC by the formation of permeable interfacial defects within the SC lipid bilayers was suggested. Also, repeated application of oleic acid induces epidermal proliferation, hyperkeratosis and sebaceous gland hyperplasia', However the exact pathomechanism was not reported. Objective : We carried out some research to observe the mechanism by which oleic acid in creases transdermal drug delivery and the effect to the skin permeability barrier and epidermis by repeated application. Methods .' In the repeated treatment group, hairless mice(6 to 8 weeks) were treated with oleic acid once a day for 7 days unilaterally, and in the single treatment group, only one time, Transepidermal water loss(TEWL) was checked at 24hour after 1, 3 and 7 days of treatment and at, 1 hour, 6 hours, 24 hours, 72 hours after single treatment. Biopsies were taken from treated and controlateral(control) sides immediately after the TEWL checks at each time for light microscopic(H & E stain) and electron microscopic studies. Results '. In the repeated treatment group, TEWL was increased by day and epidermal proliferation and hyperkeratosis were also increased. In t,he single treatment group, TEWL was highly increased in the treated site at 1 hour after treatment and decreased with time. By electronmicroscope, we observed dilated lacunae, intrcellular lipid structural abnormalities and loss of normal calcium gradient. Conclusion .' The possible domains of the epidermis interacting with oleic acid as a penetration enhancer are the lacunae and liipid bilayer by EM. The suggested pathomechanism of the epidermal changes, epidermal proliferation and hyperkeratosis was increased DNA synthesis of epidermal cells by the loss of epidermal calcium gradient in chronic barrier impairment. (Kor J Dermatol 1997;35(4): 702-711)

피부장벽에 사이토카인이 미치는 영향

최응호 ( Eung Ho Choi ),김민정 ( Min Jung Kim ),이세원 ( Se Won Lee ),박원석 ( Won Seok Park ) 한국피부장벽학회 2002 한국피부장벽학회지 Vol.4 No.1

Reviewing of medical dispute issues

최응호 ( Eung Ho Choi ) 대한피부과학회 2019 대한피부과학회 학술발표대회집 Vol.71 No.1

Recent advances on outmost skin layers of atopic dermatitis

최응호 ( Eung Ho Choi ) 대한피부과학회 2021 대한피부과학회 학술발표대회집 Vol.72 No.2

Dysfunction of the skin barrier composed of stratum corneum (SC) and tight junction is one of the pathogenesis of atopic dermatitis (AD). Congenitally or acquired skin barrier dysfunction increases allergen penetration through the SC and induces allergen sensitization more easily. Thus, AD is considered as the first step of atopic march because it can lead to asthma and allergic rhinitis with aging. Among the recent advances about the skin barrier in AD research, the research results that should be of interest are as follows. 1. A large randomized controlled trial found no evidence that daily emollient during the first year of life prevents AD in high-risk children. 2. Dry skin without eczema at 3 months is predictive for eczema at 6 months in early infancy. 3. Based on microarray study, AD displays stable and dynamic skin transcriptome signitures, which were related to clinical response to dupilumab or cyclosporine. 4. The SC, the barrier structure, is beginning to be used for AD studies to make the profiling of immune and skin barrier. 5. Prenatal particulate matter exposure with early-life skin barrier dysfunction affects early-onset persistent AD.

New insights into the pathomechanism of atopic dermatitis: The skin barrier function

최응호 ( Eung Ho Choi ) 대한피부과학회 2018 대한피부과학회 학술발표대회집 Vol.70 No.1

Research Cafe : Understanding barrier research

최응호 ( Eung Ho Choi ) 대한피부과학회 2014 대한피부과학회 학술발표대회집 Vol.66 No.2

The most important function of the skin is to provide a barrier between a harmful environment and the body. The barrier functions of the skin are mainly mediated by the stratum corneum (SC). Even minor damages to the SC can result in abnormalities in water and electrolyte balance, easier susceptibility to cutaneous infection, and cutaneous and systemic inflammatory responses. Since the concept of skin barrier was suggested by Professor Peter Elias of UC San Francisco, USA, his laboratory and colleagues have expanded the fields of barrier research. They described in detail the structure and function of the SC, and the factors regulating the formation of the SC and its abnormalities. A brief history of the development of concepts of the SC from dead cell layers to dynamic living layers functioning as a biosensor will be introduced. The structure of the SC with the lipid membrane and protein components, their integration, the role of pH and lipid processing, the various functions including permeability barrier, antimicrobial barrier, hydration and vitamin D formation will be also presented. Additionally, the effect of aging, psychological stress, and cutaneous diseases such as atopic dermatitis on the skin barrier will presented. Practical methods for barrier researches applying to mouse or human skin will be briefly prepared. I hope the audiences are going to have an interest on barrier research and a new idea for improving skin barrier function, and a willingness to start their own researches as soon as possible.

Skin barrier alteration under psychological stress

최응호 ( Eung Ho Choi ) 한국피부장벽학회 2009 한국피부장벽학회지 Vol.11 No.2

Atopic dermatitis and psoriasis are adversely affected by psychological stress (PS), but the pathophysiologic link between PS and disease expression remains unclear. Some series of recent studies showed that PS decreases epidermal proliferation and differentiation, impairs permeability barrier homeostasis, decreases stratum corneum (SC) integrity and increases group A Streptococcal pyogenes cutaneous infection in mice. PS also increases the production of endogenous glucocorticoids (GC), and both systemic and topical GC cause adverse effects on epidermal structure and function similar to those observed with PS. By the mechanisms PS decreases epidermal cell proliferation, impairs epidermal differentiation, decreases the density and size of corneodesmosomes (CD), and decreases an expression of epidermal antimicrobial peptide (AMP). Barrier dysfunction is resulted from decreased production and secretion of lamellar bodies (LB), which in turn, could be attributed to a decrease of epidermal lipid synthesis. Topical physiologic lipids mixture composed of equimolar cholesterol, ceramides and free fatty acids, normalized barrier homeostasis, SC integrity and AMP level in PS mice. Therefore, PS inhibition of epidermal lipid synthesis results in decreased LB production and secretion, as well as decreased CD and AMP delivery to LB, which are compromising permeability barrier homeostasis, SC integrity and antimicrobial defense. To confirm the hypothesis that increased endogenous GC in PS mediates its adverse cutaneous effects, RU-486 and antalarmin were used. RU-486, a GC receptor antagonist, inhibits GC action, and antalarmin, a corticotrophin releasing hormone (CRH) receptor antagonist, prevents increased GC production in the face of PS. Inhibition of either GC action or production prevents the PS-induced decline in keratinocyte proliferation and differentiation, impairment in permeability barrier homeostasis, decrease in SC integrity and decrease of AMP expression. Thus, many of the adverse effects of PS on the structure and function of epidermal permeability and antimicrobial barrier can be attributed to increased endogenous GC. Conversely, approaches that either reduces GC production or action might benefit skin diseases provoked or exacerbated by PS. Physiologic lipid replacement, PS reduction such as aroma therapy and meditation, and GC receptor antagonists could also be beneficial in PS induced, barrier associated dermatoses.

경부에 발생한 이소성 타액선 조직

최응호(Eung Ho Choi),조성환(Sung Whan Cho),이승헌(Sung Hun Lee) 대한피부과학회 1989 대한피부과학회지 Vol.27 No.6

An 8-year-old girl had a rice sized erythematous nodule secreting mucoid fluid situated above the right sternoclavicular joint area since birth. Histopathological findings of the lesion revealed predominant mucous acini, serous acini, demilunes of mixed acini and excretory ducts in the deep dermis compatible with salivary gland. Electron microscopic findings revealed a lumen and serous cells containing serous granules and rough endoplasmic reticulurn. Recurrence has not been noted following total excision of the nodule.

Pseudoceramide(PC104)로 대체한 지질혼합물을 함유한 보습제의 노인성 건조피부에 대한 효과

최응호 ( Eung Ho Choi ),박원석 ( Won Seok Park ),손의동 ( Eui Dong Son ),안성구 ( Sung Ku Ahn ),이승헌 ( Seung Hun Lee ) 한국피부장벽학회 2001 한국피부장벽학회지 Vol.3 No.1

Symposium 2-4 (SYP 2-4) : Skin barrier and microbiome in atopic dermatitis

최응호 ( Eung Ho Choi ) 대한피부과학회 2016 대한피부과학회 학술발표대회집 Vol.68 No.1

Recently, a defect in skin barrier has been formulated as a pathogenesis of atopic dermatitis (AD) development. Congenitally impaired skin barrier as a main cause of AD can increase allergen penetration through stratum corneum (SC) and then induce allergen sensitization easier. Therefore, AD has been considered as a first step of atopic march since it can eventually progress to asthma and allergic rhinitis with aging. So far, the barrier related pathogenesis of AD have been summarized as below. First, loss of function mutation of filaggrin gene is associated with the development of AD presenting early onset, severe symptoms, frequent occurrence of asthma and progression to adult AD, because filaggrin is a key protein of the epidermal differentiation complex of the SC, a major physical barrier. Second, AD skin shows a deficiency of ceramide which mostly consist SC intercellular lipid lamellae. Third, the imbalance between serine proteases (SP) and SP inhibitors caused by their genetic defects was reported in AD. Continued SP activity due to congenital defect of SP inhibitor disrupts barrier integrity and delays barrier recovery. Fourth, tight junction is also congenitally impaired in AD, which also permits easier allergen penetration and sensitization in AD. Gut microbiome such as Akkermansia was not observed in AD patients compared to healthy controls. Akkermansia produces short chain fatty acids in the gut mucosa, which contribute to the inhibition of inflammation. Therefore, a reduction of Akkermansia in the gut mucosa of infants might result in AD development. No difference in a diversity of skin microbiome was observed between AD patients and control subjects. Staphylococcus aureus was more frequently observed in AD patients compared to control subjects, but not significant. On the contrary, Lactbacillus salivarius was not observed in the skin of AD patients.