Disease relevance of Toxicodendron

• Poison oak, ivy, and sumac dermatitis is a T-cell-mediated reaction against urushiol, the oil found in the leaf of the plants [1].
• Allergic contact dermatitis to Toxicodendron radicans (poison ivy) is mediated by the hapten urushiol [2].
• 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].
• Mice epicutaneously painted with components of poison ivy urushiol oil exhibit contact sensitivity (as detected by ear swelling reactions) that persist for about 25 days [4].
• 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 [5].

Psychiatry related information on Toxicodendron

• METHOD: We assessed rash incidence in 100 patients with DSM-IV bipolar disorder instructed, for their first 3 months taking lamotrigine, to avoid other new medicines and new foods, cosmetics, conditioners, deodorants, detergents, and fabric softeners, as well as sunburn and exposure to poison ivy/oak [6].

High impact information on Toxicodendron

• Failure of a tapering dose of oral methylprednisolone to treat reactions to poison ivy [7].
• 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 [8].
• Moreover, urushiol, the toxic principle of poison ivy, but not pentadecanylcatechol, its inert analogue, showed synergy with ionomycin [9].
• As urushiol is also a known PK-C agonist, we asked if topical application of a poison ivy/oak mixture could directly induce epidermal KC ICAM-1 expression [3].
• The allergen was previously isolated and characterized as a 3-(pentadecyl-10-enyl) catechol, a molecule belonging to the urushiol group of allergens isolated from poison ivy and poison oak plants [10].

Chemical compound and disease context of Toxicodendron

• Its activity has been evaluated using the vasoconstrictor assay and the poison ivy test (rhus dermatitis) in 19/20 healthy volunteers of either sex [11].
• Evaluation of delayed hypersensitivity: from PPD to poison ivy [12].

Biological context of Toxicodendron

• These T-cell clones had a CD8+ (T8+) phenotype and proliferated specifically to both extracts of Toxicodendron radicans (poison ivy) leaves and pure urushiol [13].

Anatomical context of Toxicodendron

• In vitro studies of poison oak immunity. I. In vitro reaction of human lymphocytes to urushiol [1].
• Moreover, epidermal keratinocytes appear to play a pre-eminent role in the skin, serving as transducing elements converting exogenously applied low-molecular-weight chemical stimuli such as phorbol ester and urushiol (the active ingredient in poison ivy extracts) into the production of endogenously derived immunoregulatory proteins [14].
• TIM is based on the observation that skin contact sensitizing agents such as poison ivy, poison oak and dinitrochlorobenzene (DNCB) are potent stimulants of the cellular immune system that combats viruses and other pathogens [15].

Associations of Toxicodendron with chemical compounds

• Liposomes containing 3-n-pentadecylcatechol induce tolerance to toxicodendron [16].
• Moreover, compound 9 exhibited tolerogenic properties to sensitization by poison ivy allergens, i.e. mice pretreated with perfluorinated compounds could not be sensitized to PDC [17].
• Double-headed haptens with pyrocatechol (poison ivy like) and methylene lactone functional groups: a search for skin-tolerance inducers [18].
• 3-(Tridecafluoroundecyl)catechol (8) and 3-(nonafluoropentadecyl)catechol (9), perfluorinated analogues of pentadecylcatechol (PDC), a constituent of poison ivy, have been synthesized [17].
• Saturated analogues of poison ivy and oak allergens (3-alkylcatechols), i.e. trans,trans-3-alkyl-1,2-cyclohexanediols (alkyl = CH3, n-C5H11, n-C10H21, n-C15H31), have been prepared and used to sensitize guinea pigs [19].

Gene context of Toxicodendron

• Keratinocyte interleukin-10 expression is upregulated in tape-stripped skin, poison ivy dermatitis, and Sezary syndrome, but not in psoriatic plaques [20].
• 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 [21].
• The poison ivy picker of Pennypack Park: the continuing saga of poison ivy [22].
• Sun-damaged skin, psoriatic lesional skin, and skin from lesions of poison ivy dermatitis, however, have increased levels of telomerase activity compared to sun-protected skin, although less than that detected in tumor tissue [23].
• 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) [24].

Analytical, diagnostic and therapeutic context of Toxicodendron

• Preservation of allergic contact dermatitis to poison ivy (urushiol) in late HIV disease. The implications and relevance to immunotherapy with contact allergens [25].

References