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1.
PLoS One ; 16(12): e0261253, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34914754

RESUMEN

BACKGROUND: Xerosis cutis or dry skin is a highly prevalent dermatological disorder especially in the elderly and in patients with underlying health conditions. In the past decades, numerous molecular markers have been investigated for their association with the occurrence or severity of skin dryness. The aim of this review was to summarize the molecular markers used in xerosis cutis research and to describe possible associations with different dry skin etiologies. METHODS: We conducted a systematic review of molecular markers of xerosis cutis caused by internal or systemic changes. References published between 1990 and September 2020 were searched using 'MEDLINE', 'EMBASE' and 'Biological abstracts' databases. Study results were summarized and analyzed descriptively. The review protocol was registered in PROSPERO database (CRD42020214173). RESULTS: A total of 21 study reports describing 72 molecules were identified including lipids, natural moisturizing factors (NMFs), proteins including cytokines and metabolites or metabolic products. Most frequently reported markers were ceramides, total free fatty acids, triglycerides and selected components of NMFs. Thirty-one markers were reported only once. Although, associations of these molecular markers with skin dryness were described, reports of unclear and/or no association were also frequent for nearly every marker. CONCLUSION: An unexpectedly high number of various molecules to quantify xerosis cutis was found. There is substantial heterogeneity regarding molecular marker selection, tissue sampling and laboratory analyses. Empirical evidence is also heterogeneous regarding possible associations with dry skin. Total free fatty acids, total ceramide, ceramide (NP), ceramide (NS), triglyceride, total free amino acids and serine seem to be relevant, but the association with dry skin is inconsistent. Although the quantification of molecular markers plays an important role in characterizing biological processes, pathogenic processes or pharmacologic responses, it is currently unclear which molecules work best in xerosis cutis.


Asunto(s)
Epidermis/patología , Enfermedades Cutáneas Eccematosas/genética , Piel/patología , Biomarcadores , Ceramidas , Enfermedades del Tejido Conjuntivo/patología , Epidermis/metabolismo , Ácidos Grasos no Esterificados , Humanos , Lípidos , Piel/metabolismo , Enfermedades de la Piel/genética , Enfermedades de la Piel/patología , Enfermedades Cutáneas Eccematosas/patología , Fenómenos Fisiológicos de la Piel/genética
2.
Cell Immunol ; 284(1-2): 163-71, 2013.
Artículo en Inglés | MEDLINE | ID: mdl-23978680

RESUMEN

Nickel (Ni) can cause delayed-type hypersensitivity reactions, which are thought to be mediated by the accumulation of T cells into inflamed skin. Accumulated T cells at the developmental stages in metal allergy are poorly characterized because a suitable animal model has not been established. To investigate the accumulated T cells in allergic inflamed skin, we generated a novel murine model of Ni-induced allergy. The murine model of Ni allergy was induced by two sensitizations of Ni plus lipopolysaccharide solution into the groin followed by three challenges with Ni solution into the footpad. Here we show that a specific TCR repertoire bearing Vα14Jα18, called natural killer (NK) T cells, was expanded monoclonally in BALB/c or C57BL/6 mice. Accumulation of NKT cells was characterized as CD4(+) or CD4(-)CD8(-) T cells. These results suggested that NKT cells are major pathogenic T cells at the elicitation phase of Ni allergy.


Asunto(s)
Hipersensibilidad Tardía/inmunología , Células T Asesinas Naturales/inmunología , Níquel/toxicidad , Receptores de Antígenos de Linfocitos T alfa-beta/inmunología , Enfermedades Cutáneas Eccematosas/inmunología , Animales , Modelos Animales de Enfermedad , Hipersensibilidad Tardía/inducido químicamente , Hipersensibilidad Tardía/genética , Inmunohistoquímica , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos C57BL , Células T Asesinas Naturales/efectos de los fármacos , Níquel/inmunología , ARN Mensajero/química , ARN Mensajero/genética , Receptores de Antígenos de Linfocitos T alfa-beta/genética , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Enfermedades Cutáneas Eccematosas/inducido químicamente , Enfermedades Cutáneas Eccematosas/genética
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