Disease relevance of Urushiol

• Allergic contact dermatitis to Toxicodendron radicans (poison ivy) is mediated by the hapten urushiol [1].
• Poison oak, ivy, and sumac dermatitis is a T-cell-mediated reaction against urushiol, the oil found in the leaf of the plants [2].
• 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 [1].
• The ability of small molecules such as urushiol, present as a wax on the poison ivy leaf surface, to cause allergic contact dermatitis (rhus dermatitis) has fascinated immunologists for decades [3].
• To test this hypothesis we investigated the effect of drugs that modify the fatty acid metabolism on urushiol-induced contact dermatitis in mice [4].

High impact information on Urushiol

• Finally, certain CD8+ T cells recognized urushiol in the absence of processing [5].
• The antigen processing requirements for urushiol, the immunogen of poison ivy (Toxicodendron radicans), were tested by presentation of urushiol to cultured human urushiol-responsive T cells [5].
• In contrast, presentation of urushiol to CD4+ T cells was inhibited by monensin but not by brefeldin A [5].
• 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 [1].
• In vitro studies of poison oak immunity. I. In vitro reaction of human lymphocytes to urushiol [2].

Chemical compound and disease context of Urushiol

• Profound alterations in the dermal microvasculature and the closely related fixed tissue mast cells were observed in allergic contact dermatitis reactions to dinitrochlorobenzene and urushiol in man [6].
• Pro-Q was significantly effective in reducing the irritation from sodium lauryl sulfate but did not prevent the allergic reaction to urushiol [7].
• Contact sensitivity with properties of delayed-type hypersensitivity (DTH) can be induced in mice by 3-heptadecylcatechol (HDC, a component of poison oak urushiol oil) [8].
• The objective of the studies was to demonstrate that the contact sensitivity (CS) response to poison ivy/oak could be downregulated following treatment with a monoclonal antibody (mAb) reacting with the allergen urushiol [9].

Biological context of Urushiol

• The results have established that specific immune tolerance to poison ivy urushiol is induced following 2 epicutaneous applications of the PDC analog [10].
• These T-cell clones had a CD8+ (T8+) phenotype and proliferated specifically to both extracts of Toxicodendron radicans (poison ivy) leaves and pure urushiol [11].
• Induction of suppressor T cells for lymph node cell proliferation after contact sensitization of mice with a poison oak urushiol component [8].
• A study of cross-reactions between mango contact allergens and urushiol [12].
• Quantitative structure-activity relationships for skin sensitization potential of urushiol analogues [13].

Anatomical context of Urushiol

• A blastogenesis assay employing peripheral blood lymphocytes obtained from humans sensitized to urushiol is described [2].
• Urushiol introduced into the in vitro culture on autologous lymphocytes, erythrocytes and heterologous erythrocytes produces equal results as measured by the optimal urushiol dose, the intensity of reaction, and the frequency of positive reactors [2].
• Although untreated keratinocytes expressed the 31-kDa form of the protein, 17.5-kDa IL-1beta was easily detected in keratinocytes and keratinocyte supernatants treated with either urushiol or the irritant chemicals [14].
• Fixed antigen-presenting cells were unable to present urushiol to human CD8+ urushiol-specific T cells [15].
• Suppression was triggered specifically by urushiol and required MHC compatibility both for the antigen-presenting cells and the responding B cells [16].

Associations of Urushiol with other chemical compounds

• Baseline levels of ICE mRNA were detected in keratinocyte cultures devoid of Langerhans cells and were up-regulated by nontoxic concentrations of the reactive hapten urushiol and by the irritant chemicals sodium lauryl sulfate and PMA [14].
• Attempts to characterize potential biologically important covalent interactions between electrophilic quinones derived from catechols present in poison oak/ivy (urushiol) and biomacromolecules have led to the analysis of model reactions involving sulfur and amino nucleophiles with 3-heptadecylbenzoquinone [17].
• The application of a sensitizing dose of urushiol on a dinitrofluorobenzene (DNFB)-treated skin area significantly diminished the intensity of the urushiol challenge test in guinea pigs [18].
• In situ changes in the relative abundance of human epidermal cytokine messenger RNA levels following exposure to the poison ivy/oak contact allergen urushiol [19].
• A synthesis of (15:1)-urushiol, urushiol monoene, 3-[(Z)-pentadec-8-enyl] catechol, 1,2-dihydroxy-3-[(Z)-pentadec-8-enyl] benzene, one of the toxic principles of Rhus toxicodendron and of Rhus vernicifera is described [20].

Gene context of Urushiol

• Anergic CD8+ cells were viable and able to proliferate in response to IL-2, but not in response to urushiol [15].
• Proliferation of CD8+ T cells in response to urushiol was blocked by CTLA4Ig, a recombinant fusion protein that blocks CD28/B7 interactions [15].
• IFN-gamma and TNF-alpha are involved in urushiol-induced contact hypersensitivity in mice [21].
• On cultured KCs, urushiol directly induced ICAM-1 expression but not HLA-DR [3].
• In this report, in situ hybridization was used to detect the messenger RNAs for interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) in samples of human skin prior to and at various times after application of urushiol, the immunogenic component of poison ivy/oak [19].

Analytical, diagnostic and therapeutic context of Urushiol

• Autoreactive T cells that proliferated to autologous irradiated PBMC were also enriched in skin lesions relative to blood in 5/5 urushiol patch tests [22].
• Serum IgG immunoglobulin fractions from human subjects hyposensitized to poison ivy/oak by oral administration of urushiol suppressed the induction of delayed-type hypersensitivity (DTH) responses in mice to this hapten [23].
• Preservation of allergic contact dermatitis to poison ivy (urushiol) in late HIV disease. The implications and relevance to immunotherapy with contact allergens [24].

References