These being the concentration of cylindrospermopsin was well above that likely to be encountered in natural waters (see following discussion); barrier function was disrupted by tape-stripping during the induction phase (removal of the stratum corneum by tape-stripping stimulates the release of pre- formed IL-1α and other inflammatory cytokines from the epidermis [ 27 , 28 ]); a vehicle (70% ethanol) was used to aid the transport of soluble factors across the epidermis (matrix effects can be highly significant determinants of the potency of allergens, with reported variability of more than two orders of magnitude due to different vehicles [ 29 ]); and mice were immunologically primed to respond to sensitisers by use of Freund's adjuvant and hypervitaminosis-A (vitamin A induces epidermal hyperplasia in mice; most cell-mediated immune responses are stimulated by vitamin-A supplementation [ 30 ]).
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Primary irritant and delayed-contact hypersensitivity reactions to the freshwater cyanobacterium Cylindrospermopsis raciborskii and its associated toxin cylindrospermopsin.
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