Fawzy, M. M., M. A. I. El-latif, R. Hegazy, A. Tawdy, and I. Katayama, Expression of Langerhans cells, dermal dendritic cells, and plasmacytoid dendritic cells in early stage mycosis fungoides: a case–control study, , vol. 11, issue 3: LWW, pp. 208 - 214, 2014. Abstract
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Gamal, S. M., and M. I. A. Abd El-Latif, "Sex differences in the immune profile and its relation to clinical manifestations in systemic lupus erythematosus patients", Journal of the Egyptian Women’s Dermatologic Society, vol. 11, issue 2, 2014. AbstractWebsite

BackgroundSystemic lupus erythematosus (SLE) is a heterogeneous, multisystemic autoimmune disease of unknown etiology. Men and women may show variable clinical and laboratory features, which may affect the prognosis. Several studies showed a relation between the immune profiles and the clinical and laboratory features in such patients.ObjectiveTo study the sex differences in the immune profile in a cohort of SLE patients.
Patients and methodsMedical records of 199 patients, 147 female SLE patients (group 1) and 52 male SLE patients (group 2), attending the Rheumatology and Rehabilitation Outpatient Clinic of Cairo University Hospitals were reviewed and compared retrospectively for demographic data, clinical features of the disease, laboratory features and immune profile.
ResultsThe prevalence of alopecia was significantly higher in group 1, whereas the prevalence of nephritis was significantly higher in group 2. There was a significant increase in the mean level of serum creatinine, and a tendency towards a lower mean platelet count in group 2. The positivity for antinuclear antibody and antidouble-stranded DNA (anti-dsDNA) was higher in group 2, whereas the positivity for anti-Ro, anti-La and anticardiolipin was higher in group 1. Low complement 3 (C3) and complement 4 (C4) were observed more often in group 1. None of these differences was statistically significant except for C3. A significant association was found between nephritis and anti-dsDNA in both groups, between photosensitivity and anti-Ro in group 1 and between photosensitivity and anti-La in group 2.
ConclusionAlthough the immune profile may show some differences between male and female lupus patients, most of these differences were however nonsignificant, apart from a low C3 in female patients with SLE.

El-Darouti, M. A., S. A. Marzouk, N. Nabil, M. R. E. Abdel-Halim, M. H. M. El-Komy, and M. Abdel-Latif, "Pachyonychia congenita: treatment of the thickened nails and palmoplantar circumscribed callosities with urea 40% paste.", Journal of the European Academy of Dermatology and Venereology : JEADV, vol. 20, issue 5, pp. 615-7, 2006 May. Abstract
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Murota, H., M. Izumi, M. I. A. Abd El-Latif, M. Nishioka, M. Terao, M. Tani, S. Matsui, S. Sano, and I. Katayama, "Artemin causes hypersensitivity to warm sensation, mimicking warmth-provoked pruritus in atopic dermatitis.", The Journal of allergy and clinical immunology, vol. 130, issue 3, pp. 671-682.e4, 2012 Sep. Abstract

BACKGROUND: Itch impairs the quality of life for many patients with dermatoses, especially atopic dermatitis (AD), and is frequently induced by a warm environment.

OBJECTIVE: To determine the mechanism underlying itch induction by warmth, we focused on artemin, a member of glial cell line-derived neurotrophic factors (GDNFs).

METHODS: A gene array assay revealed that artemin was expressed in substance P-treated dermal fibroblasts. The expression of artemin in healthy and AD-lesional skin was evaluated with immunohistochemistry and in situ hybridization. The impact of fibroblast-derived artemin on the proliferation and morphology of neural cell was investigated in vitro. To confirm the involvement of artemin in skin sensibility, wild-type and GDNF family receptor α3 knockout mice were employed for sensory examination.

RESULTS: Artemin-expressing fibroblasts accumulated in skin lesions of patients with AD. Artemin induced cell proliferation of a neuroblastoma cell line in vitro, and intradermal injection of artemin in mice resulted in peripheral nerve sprouting and thermal hyperalgesia. Artemin-treated mice demonstrated scratching behavior in a warm environment, but mice deficient for GDNF family receptor α3, a potent artemin receptor, did not show this behavior. Furthermore, the escaping response to heat stimulus was attenuated in GDNF family receptor α3 knockout mice, suggesting that artemin may contribute to sensitivity to heat.

CONCLUSION: These data suggest that dermal fibroblasts secrete artemin in response to substance P, leading to abnormal peripheral innvervation and thermal hyperalgesia. We hypothesize that artemin lowers the threshold of temperature-dependent itch sensation and might therefore be a novel therapeutic target for treating pruritic skin disorders, including AD.

Yang, F., M. Tanaka, M. Wataya-Kaneda, L. Yang, A. Nakamura, S. Matsumoto, M. Attia, H. Murota, and I. Katayama, "Topical application of rapamycin ointment ameliorates Dermatophagoides farina body extract-induced atopic dermatitis in NC/Nga mice.", Experimental dermatology, vol. 23, issue 8, pp. 568-72, 2014 Aug. Abstract

Atopic dermatitis (AD), a chronic inflammatory skin disease characterized by relapsing eczema and intense prurigo, requires effective and safe pharmacological therapy. Recently, rapamycin, an mTOR (mammalian target of rapamycin) inhibitor, has been reported to play a critical role in immune responses and has emerged as an effective immunosuppressive drug. In this study, we assessed whether inhibition of mTOR signalling could suppress dermatitis in mice. Rapamycin was topically applied to inflamed skin in a murine AD model that was developed by repeated topical application of Dermatophagoides farina body (Dfb) extract antigen twice weekly for 7 weeks in NC/Nga mice. The efficacy of topical rapamycin treatment was evaluated immunologically and serologically. Topical application of rapamycin reduced inflammatory cell infiltration in the dermis, alleviated the increase of serum IgE levels and resulted in a significant reduction in clinical skin condition score and marked improvement of histological findings. In addition, increased mTOR phosphorylation in the lesional skin was observed in our murine AD model. Topical application of rapamycin ointment inhibited Dfb antigen-induced dermatitis in NC/Nga mice, promising a new therapy for atopic dermatitis.

Murota, H., M. A. El-latif, T. Tamura, and I. Katayama, "Olopatadine hydrochloride decreases tissue interleukin-31 levels in an atopic dermatitis mouse model.", Acta dermato-venereologica, vol. 94, issue 1, pp. 78-9, 2014 Jan. Abstract
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Abd El-Latif, M. I. A., H. Murota, M. Terao, and I. Katayama, "Effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor and low-density lipoprotein on proliferation and migration of keratinocytes", British Journal of Dermatology, vol. 163, no. 1: Blackwell Publishing Ltd, pp. 128–137, 2010. AbstractWebsite

Background  Keratinocytes can obtain cholesterol either by de novo synthesis or by extraction, primarily from low-density lipoprotein (LDL). LDL is internalized following binding to the LDL receptor (LDLR). Because LDLR is expressed at a higher level in the cells of the basal layer of the epidermis, it might be assumed that LDLR upregulation is associated with keratinocyte proliferation. However, the effect of LDLR stimulation on keratinocyte function remains unclear.Objectives  To investigate the effects and mechanism of action of pitavastatin and effects of LDL on proliferation and migration of keratinocytes.Methods  Pitavastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, was used to induce upregulation of LDLR. LDLR expression was evaluated by immunofluorescence staining, fluorescence-activated cell sorting, immunohistochemical staining and real-time polymerase chain reaction (PCR). HaCaT cells and normal human keratinocytes (NHKs) were used for evaluation of migration. 5-Bromo-2′-deoxyuridine incorporation was used to evaluate keratinocyte proliferation and differentiation. C57BL6 mice were used for in vivo evaluation of the effect of topical pitavastatin or lovastatin.Results  Pitavastatin was most effective in LDLR induction at a concentration of 1 μmol L−1 in NHKs. Real-time PCR showed that pitavastatin significantly increased LDLR and liver X receptor (LXR) β mRNA expression in these cells. Similar results were obtained in vivo. However, pitavastatin had no effect on the migration of NHKs. After the addition of LDL and/or mevalonate concomitantly with pitavastatin to NHK cultures, or topical application of pitavastatin on mouse skin, keratinocyte proliferation was significantly increased.Conclusions  Pitavastatin significantly upregulates LDLR in both NHKs and C57BL6 mouse skin, resulting in increased keratinocyte proliferation. LXRβ may be involved in the pitavastatin-induced keratinocyte proliferation.

Murota, H., M. A. El-latif, T. Tamura, T. Amano, and I. Katayama, Olopatadine Hydrochloride Improves Dermatitis Score and Inhibits Scratch Behavior in NC/Nga Mice, , vol. 153, issue 2, pp. 121 - 132, 2010. Abstract

Background: Control of itch is an important issue in the treatment of atopic dermatitis (AD). Itch is mediated by a variety of pruritogens, including histamine, and promoted by neurite outgrowth in the epidermis of AD patients, probably due to the release of nerve growth factor. Objectives: We investigated the effects of orally administered olopatadine hydrochloride (olopatadine) on itching, itching mediators, and neuritogenic action in a mouse model. Materials and Methods: NC/Nga mice were treated topically with Dermatophagoides farinae body (Dfb) extract twice weekly for 4 weeks to induce AD-like lesions. They were concomitantly given oral olopatadine, distilled deionized water, or topical tacrolimus during the last 2 weeks. Results: Olopatadine significantly suppressed scratching, improved the dermatitis score, inhibited neurite outgrowth, and decreased the elevated inflammatory markers, growth factors and histamine content in the lesional skin, and serum concentration of Dfb-specific IgE. Notably, olopatadine treatment increased semaphorin 3A expression in the epidermis. Conclusions: Our study confirms the pleiotropic effects of olopatadine, i.e. inhibition of inflammation and neurite extension into the epidermis.

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