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Effectiveness of various barrier preparations in preventing and/or ameliorating experimentally produced Toxicodendron dermatitis.

BACKGROUND: Despite extensive research on hyposensitization and prior application of topical barrier preparations, efforts to prevent Toxicodendron dermatitis have been only minimally successful. OBJECTIVE: Seven different barrier creams were evaluated for topical protection against experimentally produced Toxicodendron dermatitis in a randomized, double-blind study. METHODS: Twenty patients had the seven barrier creams randomly applied to eight test sites (one untreated area as control) on each forearm before application of the Toxicodendron extract. Development of Toxicodendron dermatitis was followed for 8 days, with measurements of erythema, induration, vesiculation, and global severity taken at each site on days 1, 2, 3, 4, and 7 after Toxicodendron application. RESULTS: The barrier creams Stokogard, Hollister Moisture Barrier, and Hydropel significantly reduced the erythema, induration, and global severity of Toxicodendron dermatitis and did not differ from each other. The percent reductions in global dermatitis severity per day of assessment for the seven barriers in order of effectiveness were as follows: Stokogard, 59%; Hollister Moisture Barrier, 52%; Hydropel, 48%; Ivy Shield, 22%; Shield Skin, 13%; Dermofilm, 13%; and Uniderm, -9%. During the 8-day period, a significantly greater number of test sites pretreated with Stokogard, Hollister Moisture Barrier, and Hydropel were free of dermatitis compared with control sites and sites treated with the other four barriers. CONCLUSION: The results indicate that Stokogard, Hollister Moisture Barrier, and Hydropel are effective in the prevention of Toxicodendron dermatitis.

Administration, Cutaneous

New GLC analysis of urushiol congeners in different plant parts of poison ivy, Toxicodendron radicans.

Methods are presented for the direct GLC analysis of the catechol C15 alkenyl side-chain congeners contained in the urushiol fraction of poison ivy (Toxicodendron radicans) and the C17 homologs of poison oak (Toxicodendron diversilobum). A number of liquid phases were investigated and demonstrated varying degrees of separation. The methods developed were applied to the analysis of the urushiol fractions obtained from different plant parts of poison ivy. The effects of extraction before and after drying demonstrated tht a larger percentage of urushiol was obtained when the fresh plant material was extracted with ethanol.

Catechols

Quantitation and cloning of human urushiol specific peripheral blood T-cells: isolation of urushiol triggered suppressor T-cells.

A limiting dilution assay was developed to quantitate urushiol (the antigen of poison ivy; Toxicodendron radicans) specific T cells from peripheral blood of a patient with a history of rhus (poison ivy) dermatitis. It was found that maximal sensitivity with minimal nonspecific proliferation could be produced with the use of 5 U/ml of recombinant IL2 added to the assay on day 6. This donor was found to have a frequency of urushiol specific peripheral blood T cells of (1/2935). Five interleukin 2 (IL2) dependent urushiol specific T-cell clones were generated from the peripheral blood of this patient. These T-cell clones had a CD8+ (T8+) phenotype and proliferated specifically to both extracts of Toxicodendron radicans (poison ivy) leaves and pure urushiol. Pentadecylcatechol was an inferior antigen, only stimulating proliferation of one clone. The ability of all clones to proliferate to pure urushiol, despite their having been induced with leaf extract, suggests that urushiol, or closely related catechols, represent the only allergenic constituents of Toxicodendron radicans. Lymphokine production in response to antigen varied between (0.6-5.0) units/ml of interleukin 2 (IL2) and (1.0-120) units/ml of gamma interferon. Although none of the clones showed significant cytotoxicity against NK targets, three of five lines showed considerable cytotoxicity against concanavalin A treated (lectin approximated) targets. However, cytotoxicity for rhus conjugated autologous targets was not detected. It was found that several of these CD8+ clones could suppress IgG production in the presence of rhus antigen. The isolation of these T-cells from peripheral blood several months after rhus dermatitis suggests that these clones may have a role in down regulating delayed hypersensitivity to urushiol.

Catechols

Contact dermatitis from Grevillea 'Robyn Gordon'.

Grevillea 'Robyn Gordon' is an Australian hybrid plant which may cause allergic contact dermatitis. Over the past 8 years, it has been planted extensively in Australia and is now being exported to the United States and other Western countries. Recently, an explosion in incidence of contact dermatitis due to this plant has been seen. 24 patients who were suspected of being sensitive to it were patch tested to fresh plant and extracts with confirmation of sensitivity. A cross sensitivity to Toxicodendron was demonstrated clinically and on patch testing. The allergen in Toxicodendron, 3 pentadecylcatechol, is closely linked in chemical structure to 5-pentadecylresorcinol, present in Grevillea banksii and tridecylresorcinol in Grevillea robusta. Patch testing in patients sensitive to Grevillea 'Robyn Gordon' with tridecylresorcinol produced positive reactions, thus implicating the sensitizing rôle of long chain alkyl resorcinols in Grevillea 'Robyn Gordon' allergy. There is a likelihood that this sensitizing potential extends to other plants of the Grevillea genus, e.g., Grevillea robusta. With the spread of Grevillea 'Robyn Gordon' to other markets, this problem will become increasingly common.

Adult

Characterization of poison oak urushiol.

Procedures are described that were used in the isolation and characterization of urushiol components reported to be the allergenic constituents of poison oak, Toxicodendron diversilobum. Characterization of these components by spectral techniques indicated they are unsaturated congeners of 3-heptadecylcatechol, possessing one, two, or three double bonds in an unbranched C17 side chain. These components are shown to differ from those isolated from poison ivy, Toxicodendron radicans, by a - CH2CH2-unit in the unbranched alkyl side chain.

Catechols

Urushiol (poison ivy)-triggered suppressor T cell clone generated from peripheral blood.

Allergic contact dermatitis to Toxicodendron radicans (poison ivy) is mediated by the hapten urushiol. An urushiol-specific, interleukin 2 (IL-2)-dependent T cell clone (RLB9-7) was generated from the peripheral blood of a patient with a history of allergic contact dermatitis to T. radicans. This clone proliferated specifically to both leaf extract and pure urushiol. Although the clone had the phenotype CD3+CD4+CD8+, proliferation to antigen was blocked by anti-CD8 and anti-HLA-A, B, C, but not by anti-CD4, suggesting that CD4 was not functionally associated with the T cell receptor. Furthermore, studies with antigen-presenting cells from MHC-typed donors indicated that the clone was MHC class 1 restricted. RLB9-7 was WT31 positive, indicating it bears the alpha beta T cell receptor. The clone lacked significant natural killer cell activity and produced only low levels of IL-2 or gamma-interferon upon antigen stimulation. Addition of RLB9-7 to autologous peripheral blood mononuclear cells in the presence of urushiol inhibited the pokeweed mitogen-driven IgG synthesis. This suppression was resistant to irradiation (2,000 rad) and was not seen when RLB9-7 was added to allogeneic cells, even in the presence of irradiated autologous antigen-presenting cells, suggesting that suppression was MHC restricted and not mediated by nonspecific soluble factors. However, RLB9-7 cells in the presence of urushiol inhibited the synthesis of tetanus toxoid-specific IgG by autologous lymphocytes, indicating that the suppression, although triggered specifically by urushiol, was nonspecific.

Antibody Specificity

The use of human T-lymphocyte clones to study T-cell function in allergic contact dermatitis to urushiol.

Allergic contact dermatitis to poison ivy (Toxicodendron radicans) is believed to be mediated by T lymphocytes specific for the hapten urushiol. Activated T lymphocytes may produce pathology by a variety of mechanisms including direct cytotoxicity, production of lymphokines, recruitment of non-specific effector cells, non-specific cytotoxicity, and possibly autologous DR reactivity. The regulation and pathogenesis of this condition was studied by cloning and characterizing urushiol-specific T cells from the peripheral blood of patients with poison ivy dermatitis. Multiple CD8+ (T8+) urushiol-specific clones were derived. All clones that proliferated in response to a crude extract of T. radicans also proliferated in response to purified urushiol. Thus, urushiol appears to be the single immunogenic component of T. radicans resin. Pentadecylcatechol (PDC), which differs from urushiol only in the lack of unsaturated bonds in its lipophilic tail, stimulated only one of seven clones tested. This suggests that the double bonds in the C15 lipophilic tail of urushiol are required for antigenicity. Several of the CD8+ urushiol-specific clone suppressed pokeweed mitogen-induced IgG production in the presence of urushiol. Suppression was triggered specifically by urushiol and required MHC compatibility both for the antigen-presenting cells and the responding B cells. These suppressor clones were isolated from convalescent blood and may represent a mechanism for the termination of an allergic contact dermatitis.

Antigens

Unusual contact allergens from plants in the family Hydrophyllaceae.

The dermatitic constituents of the glandular hairs of plants in the family Hydrophyllaceae comprise a class of uncommon natural products called "phacelioids". The chemical structures consist of various elaborations of hydroquinone attached to a C10 to C20 prenyl chain. Certain of these compounds are equivalent to the urushiols of Toxicodendron (Rhus) in their capacity to sensitize humans. Although structurally related to the urushiols, the phacelioids do not appear to cross-react in humans either with urushiol, or between phacelioids with different prenyl chains.

Allergens

Heat treatment of Japanese lacquerware renders it hypoallergenic.

Japanese lacquer is made from the sap of the Japanese lacquer tree (Toxicodendron vernicifluum), a member of the Anacardiacae plant family. Objects painted with this material are described collectively as lacquerware. Both fresh lacquer and lacquerware may evoke allergic contact reactions ascribable to the urushiols contained therein. In this study, we have examined the effects of heating on the ability of lacquerware to elicit an allergic contact reaction. Lacquer films prepared with and without heat treatment were tested on urushiol-sensitive subjects. Patch test reactions were strongest to untreated film and decreased with increasing level of heat treatment. Assays for free urushiol in the lacquer films demonstrated that free urushiol content decreased with increasing heat treatment and that urushiols with saturated and monounsaturated alk(en)yl chains predominated.

Adult

Philodendron-induced dermatitis: report of cases and review of the literature.

Plants of the genus Philodendron, and the family Araceae, were reported as causing dermatitis as early as 1923. The allergenic compounds in philodendrons are resorcinols, which share common chemical side chains with the allergenic catechols of Toxicodendron members of the family Anacardiaceae. I report here two cases of allergic contact dermatitis to Philodendron species commonly found in the Hawaiian islands. Philodendron dermatitis, however, is not confined to tropical or subtropical areas. Exposure may occur in nursery workers in temperate climates and in the home environment worldwide.

Acute Disease

Analogues of poison ivy urushiol. Synthesis and biological activity of disubstituted n-alkylbenzenes.

The total synthesis of different isomers and analogues of poison ivy urushiol is described. These include the positional isomers 1-5 and the nitrogen-containing analogues 6 and 8 and their mesylamino derivatives 7 and 9. 3,4-Dimethoxybenzaldehyde, m-dimethoxybenzene, resorcinol, and p-dimethoxybenzene were used as starting materials for compounds 1, 2, 3, and 4, respectively. Compound 5 is prepared by catalytic hydrogenation of bilobol isolated from Ginkgo biloba. Compounds 6 and 7 were prepared from anacardic acid as the starting material while compounds 8 and 9 were prepared from phenol as the starting material. Compounds 1-9 were tested for their ability to cross-react with poison ivy urushiol in sensitized guinea pigs. Compounds 6 and 8 were reactive at the 10-microgram dose level when applied topically, while compound 1 was a skin irritant at that dose. On the other hand, compounds 2-5, 7, and 9 showed no cross-reactivity up to the 30-micrograms dose level. Structural requirements for cross allergenicity are discussed.

Animals