Cutaneous and ocular toxicology · 2026
Characterization of epidermal and dermal remodeling following skin injury by sulfur mustard in Göttingen minipigs.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Joseph Laurie B, Ozkuyumcu Kevin, Weinstock Daniel, Zhou Peihong, Croutch Claire R, Laskin Jeffrey D
Аннотация
PURPOSE: Sulfur mustard (SM) is a highly reactive chemical warfare agent that causes severe cutaneous injury, including blistering, necrosis, inflammation, and delayed wound repair. This exploratory study characterized cellular and molecular changes associated with SMinduced skin injury and repair over 60 days.
MATERIALS AND METHODS: Göttingen minipigs received a single SM exposure using a vapor cap model. Skin samples were analyzed for changes in epidermal architecture, proliferation, adhesion, differentiation, and dermal remodeling using histopathology and immunochemistry. Markers included proliferating cell nuclear antigen (PCNA), E-cadherin, keratin 10, and loricrin. Trichrome staining assessed collagen organization and extracellular matrix remodeling.
RESULTS: At 2 days post exposure, marked epidermal disruption, including degeneration and necrosis of basal and suprabasal keratinocytes, was accompanied by mild dermal edema and polymorphonuclear leukocyte infiltration. From 9 to 28 days, epidermal repair was evident, with hyperplasia, irregular stratification, and incomplete differentiation of the neoepidermis. Increased PCNA expression indicated enhanced basal keratinocyte proliferation, while reduced E-cadherin expression suggested impaired epithelial adhesion. Altered keratin 10 and loricrin localization demonstrated disrupted keratinocyte differentiation and barrier formation. Trichrome staining demonstrated dermal remodeling, including mild edema, increased cellularity, and the development of a distinct papillary-reticular interface. By 60 days, partial restoration of epidermal organization and normalization of keratin expression suggested progressive recovery.
CONCLUSIONS: SM exposure induces persistent alterations in epidermal architecture, proliferation, differentiation, adhesion, and dermal matrix organization. These findings provide preliminary insight into mechanisms underlying SM-induced skin injury and repair and support further investigation of pathways regulating epidermal regeneration and dermal remodeling.
MATERIALS AND METHODS: Göttingen minipigs received a single SM exposure using a vapor cap model. Skin samples were analyzed for changes in epidermal architecture, proliferation, adhesion, differentiation, and dermal remodeling using histopathology and immunochemistry. Markers included proliferating cell nuclear antigen (PCNA), E-cadherin, keratin 10, and loricrin. Trichrome staining assessed collagen organization and extracellular matrix remodeling.
RESULTS: At 2 days post exposure, marked epidermal disruption, including degeneration and necrosis of basal and suprabasal keratinocytes, was accompanied by mild dermal edema and polymorphonuclear leukocyte infiltration. From 9 to 28 days, epidermal repair was evident, with hyperplasia, irregular stratification, and incomplete differentiation of the neoepidermis. Increased PCNA expression indicated enhanced basal keratinocyte proliferation, while reduced E-cadherin expression suggested impaired epithelial adhesion. Altered keratin 10 and loricrin localization demonstrated disrupted keratinocyte differentiation and barrier formation. Trichrome staining demonstrated dermal remodeling, including mild edema, increased cellularity, and the development of a distinct papillary-reticular interface. By 60 days, partial restoration of epidermal organization and normalization of keratin expression suggested progressive recovery.
CONCLUSIONS: SM exposure induces persistent alterations in epidermal architecture, proliferation, differentiation, adhesion, and dermal matrix organization. These findings provide preliminary insight into mechanisms underlying SM-induced skin injury and repair and support further investigation of pathways regulating epidermal regeneration and dermal remodeling.