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Tissue injury and repair following cutaneous exposure of mice to sulfur mustard
Author(s) -
Joseph Laurie B.,
Composto Gabriella M.,
Heck Diane E.
Publication year - 2016
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.13125
Subject(s) - proinflammatory cytokine , eschar , dermis , wound healing , sulfur mustard , epidermis (zoology) , skin repair , dermal fibroblast , inflammation , granulation tissue , nitric oxide synthase , nitric oxide , chemistry , fibroblast , microbiology and biotechnology , immunology , pathology , toxicity , biology , medicine , biochemistry , anatomy , organic chemistry , in vitro
In mouse skin, sulfur mustard (SM) is a potent vesicant, damaging both the epidermis and the dermis. The extent of wounding is dependent on the dose of SM and the duration of exposure. Initial responses include erythema, pruritus, edema, and xerosis; this is followed by an accumulation of inflammatory leukocytes in the tissue, activation of mast cells, and the release of mediators, including proinflammatory cytokines and bioactive lipids. These proinflammatory mediators contribute to damaging the epidermis, hair follicles, and sebaceous glands and to disruption of the epidermal basement membrane. This can lead to separation of the epidermis from the dermis, resulting in a blister, which ruptures, leading to the formation of an eschar. The eschar stimulates the formation of a neoepidermis and wound repair and may result in persistent epidermal hyperplasia. Epidermal damage and repair is associated with upregulation of enzymes generating proinflammatory and pro‐growth/pro‐wound healing mediators, including cyclooxygenase‐2, which generates prostanoids, inducible nitric oxide synthase, which generates nitric oxide, fibroblast growth factor receptor 2, and galectin‐3. Characterization of the mediators regulating structural changes in the skin during SM‐induced tissue damage and wound healing will aid in the development of therapeutic modalities to mitigate toxicity and stimulate tissue repair processes.