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Response of Artificial Human Skin to Irritants: Cytokine and Prostaglandin Release

Cytokines have been implicated in aspects of vesicant injury/repair. This study describes responses of artificial human skin (Skin2 and EpiDerm) to chloroethyl ethyl sulfide (CEES), defined by interleukin-la (Tb-la), tumor necrosis factor-a (TNF-a) and prostaglandin E2 (PGE2) release. Skin2 and EpiD...

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Bibliographic Details
Main Authors: Bowers, W., Jr, Blaha, M, Alkhyyat, A, Walker, J
Format: Report
Language:English
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Summary:Cytokines have been implicated in aspects of vesicant injury/repair. This study describes responses of artificial human skin (Skin2 and EpiDerm) to chloroethyl ethyl sulfide (CEES), defined by interleukin-la (Tb-la), tumor necrosis factor-a (TNF-a) and prostaglandin E2 (PGE2) release. Skin2 and EpiDerm in Millicells of 6 well Costar trays containing 1ml of assay media/well were exposed to CEES (2.Omg/L, flow rate 1l/min for 2hr) in humidified air. Control tissues were exposed without CEES. Millicells containing Skin2 or EpiDerm (12/group) were transferred to fresh assay media and incubated for 22 hr. Tissues (6/group) were used for MTT tests. Media from each well were stored in liquid N2. Tb-la (RIA or EbISA), PGE2 (RIA or ETA), and TNF-a (ETA) were measured in thawed specimens. CEES significantly increased release of Tb-la (l92pg/ml plus or minus 34.9, control SSpg/ml i 16.6) and PGE2 (3,977pg/O.lml plus oir minus 1,197, control 2154lpg/O.lml plus or minus 570) from Skin21 but not TNF-a levels, with viability (MTT) 3%. Neither Tb-la nor TNF-a were elevated by CEES-exposed EpiDerm, although PGE2 was elevated (25Bpg/O.lml plus or minus 71 vs 184 plus or minus 79), viability 46%. We conclude pro-inflammatory mediators, Tb-la and PGE21 could play significant roles in CEES injury and that either fibroblasts are critical to the process, or EpiDerm, which lacks fibroblasts, is somehow more resistant.