Response of Artificial Human Skin to Irritants: Cytokine and Prostaglandin Release.
ARMY RESEARCH INST OF ENVIRONMENTAL MEDICINE NATICK MA
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Cytokines have been implicated in aspects of vesicant injuryrepair. 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 mediawell were exposed to CEES 2.OmgL, flow rate 1lmin for 2hr in humidified air. Control tissues were exposed without CEES. Millicells containing Skin2 or EpiDerm 12group were transferred to fresh assay media and incubated for 22 hr. Tissues 6group 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 l92pgml plus or minus 34.9, control SSpgml i 16.6 and PGE2 3,977pgO.lml plus oir minus 1,197, control 2154lpgO.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 25BpgO.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.
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