Innovation in prevention of poison oak contact dermatitis.

Poison oak-induced contact dermatitis poses a significant challenge due to its urushiol oil-induced allergic reactions. Conventional preventive measures like avoidance and post-exposure cleansing are often impractical, necessitating innovative strategies. This comprehensive review explores emerging technologies and formulations for preventing poison oak dermatitis. Literature search via PubMed and Covidence identified 13 relevant studies, with six discussing preventive measures. Barrier methods, including occlusive creams and protective clothing, showed promise in reducing dermatitis risk. Immunotherapy, although investigated, requires further development. Complete avoidance, while effective, is often impractical. The complexity of poison oak management underscores the need for ongoing research to develop more effective preventive measures. This review highlights the current landscape, identifies gaps in knowledge, and emphasizes the importance of continued research for improved prevention and management of poison oak-induced dermatitis.

Effects of diet on skin sensitization by nickel, poison ivy, and sesquiterpene lactones.

Skin contact or exposure to sensitizers often occurs as a consequence of occupational exposures (e.g. poison ivy in forestry), wearing jewelry (e.g. nickel), or use of cosmetics (e.g. fragrances). However, many of the known skin sensitizers or their chemical variants are also consumed orally through foods or other sources. Since oral exposure to antigenic substances can lead to tolerance, consumption of sensitizers may impact the development and potency of skin sensitization, especially if the sensitizer is consumed early in life, prior to the first skin contact. To address this issue, we have reviewed human clinical and epidemiological literature relevant to this subject and evaluated whether early oral exposures to relevant sensitizers, or their chemical variants, are associated with reduced prevalence of skin sensitization to three main allergic sensitizers - nickel, urushiols of poison ivy, and sesquiterpene lactones of chrysanthemum and other plants.

Transcriptome profiling reveals Th2 bias and identifies endogenous itch mediators in poison ivy contact dermatitis.

In the United States, poison ivy exposure is the most common naturally occurring allergen to cause allergic contact dermatitis (ACD). The immune and pruritic mechanisms associated with poison ivy ACD remain largely unexplored. Here, we compared skin whole transcriptomes and itch mediator levels in mouse ACD models induced by the poison ivy allergen, urushiol, and the synthetic allergen, oxazolone. The urushiol model produced a Th2-biased immune response and scratching behavior, resembling findings in poison ivy patients. Urushiol-challenged skin contained elevated levels of the cytokine thymic stromal lymphopoietin (TSLP), a T-cell regulator and itch mediator, and pruritogenic serotonin (5-HT) and endothelin (ET-1), but not substance P (SP) or histamine. The oxazolone model generated a mixed Th1/Th2 response associated with increased levels of substance P, 5-HT, ET-1, but not TSLP or histamine. Injections of a TSLP monoclonal neutralizing antibody, serotonergic or endothelin inhibitors, but not SP inhibitors or antihistamines, reduced scratching behaviors in urushiol-challenged mice. Our findings suggest that the mouse urushiol model may serve as a translational model of human poison ivy ACD study. Inhibiting signaling by TSLP and other cytokines may represent alternatives to the standard steroid/antihistamine regimen for steroid-resistant or -intolerant patients and in exaggerated systemic responses to poison ivy.

CD1a on Langerhans cells controls inflammatory skin disease.

CD1a is a lipid-presenting molecule that is abundantly expressed on Langerhans cells. However, the in vivo role of CD1a has remained unclear, principally because CD1a is lacking in mice. Through the use of mice with transgenic expression of CD1a, we found that the plant-derived lipid urushiol triggered CD1a-dependent skin inflammation driven by CD4(+) helper T cells that produced the cytokines IL-17 and IL-22 (TH17 cells). Human subjects with poison-ivy dermatitis had a similar cytokine signature following CD1a-mediated recognition of urushiol. Among various urushiol congeners, we identified diunsaturated pentadecylcatechol (C15:2) as the dominant antigen for CD1a-restricted T cells. We determined the crystal structure of the CD1a-urushiol (C15:2) complex, demonstrating the molecular basis of urushiol interaction with the antigen-binding cleft of CD1a. In a mouse model and in patients with psoriasis, CD1a amplified inflammatory responses that were mediated by TH17 cells that reacted to self lipid antigens. Treatment with blocking antibodies to CD1a alleviated skin inflammation. Thus, we propose CD1a as a potential therapeutic target in inflammatory skin diseases.

When your patients are itching to see you: not all hives are urticaria.

When patients present with itching and the perception that they have hives, what other processes can mimic urticaria? With the exception of urticarial vasculitis, urticaria typically lasts less than 24 to 36 hours at one site. A rash that persists longer should raise the suspicion of another inflammatory process. When the hive-like rash does not respond to antihistamines, a biopsy may reveal an alternative diagnosis. All biopsies should also be submitted for immunofluorescence to exclude atypical presentations of inflammatory bullous disease presenting with urticaria. However, even biopsies can be subject to misinterpretation and if the clinical picture does not support the biopsy, an alternative consultation with a dermatopathologist may be required. The extent of the laboratory and radiologic evaluation should be dictated by the clinician's suspicion of alternative causes for the hive(s) because rarely malignancies may present with urticaria. Common things are indeed common with urticaria and the more urticaria does not appear to be typical, the more often the clinician should consider alternative diagnoses.

Exploring the mango-poison ivy connection: the riddle of discriminative plant dermatitis.

A relationship between sensitivity to poison oak or poison ivy and mango dermatitis has been suggested by previous publications. The observation that acute allergic contact dermatitis can arise on first exposure to mango in patients who have been sensitized beforehand by contact with other urushiol-containing plants has been documented previously. We report 17 American patients employed in mango picking at a summer camp in Israel, who developed a rash of varying severity. All patients were either in contact with poison ivy/oak in the past or lived in areas where these plants are endemic. None recalled previous contact with mango. In contrast, none of their Israeli companions who had never been exposed to poison ivy/oak developed mango dermatitis. These observations suggest that individuals with known history of poison ivy/oak allergy, or those residing in area where these plants are common, may develop allergic contact dermatitis from mango on first exposure. We hypothesize that previous oral exposure to urushiol in the local Israeli population might establish immune tolerance to these plants.

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

BACKGROUND: Delayed hypersensitivity reactions (DTH) are lost with progression of HIV disease. This loss of DTH commonly occurs before the onset of opportunistic infections and is an independent predictor of disease progression. OBJECTIVE: We wanted to determine whether patients in late HIV disease with a history of allergic contact dermatitis (ACD) to poison ivy continue to react to poison ivy. METHODS: Twelve HIV+ patients with a past history of ACD to poison ivy were tested with an extract prepared from poison ivy leaves. All but 1 patient had CD4+ T cell counts < 200/microliters, and 5 patients had had an opportunistic infection. RESULTS: All 12 patients showed positive reactions ranging from mild erythema and infiltration to marked erythema with bulla formation. CONCLUSIONS: ACD is considered a variant of DTH, and as DTH results in a T helper 1 cytokine pattern. However, the antigen-specific effector cells in ACD may be more diverse than in DTH. This diversity could explain the continued reaction to some contact allergens in late disease and may be important in the use of contact allergens for immunotherapy.

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.

Age differences in poison ivy dermatitis.

In both man and animals, cell-mediated immunity diminishes with advanced age. Because poison ivy is a very common allergy, we evaluated age-associated differences in the contact allergic reaction to Rhus. Oleoresin patch tests were applied to two age cohorts (18-25 versus 65-84) each of 14 healthy white subjects. In the elderly, the allergic reaction developed more slowly, the inflammatory response at peak was greatly diminished and the dermatitis lasted longer and seemed to be more pruritic.

Toxicodendron antigen patch test. Degrees of inflammation observed after various time intervals.

Allergic contact dermatitis was elicited with Toxicodendron antigen and the patch test site examined at various time intervals up to one week. The degree of inflammation was rather constant during the observation period. The mean erythema score at 168 hours was not significantly different from the score at 24 hours. These data support the use of a delayed (96-hour) patch test reading as a guide to discriminating between allergic and irritant patch test reactions.

Nonenzymic spectrophotometric determination of potential poison ivy cross-reactors.

I describe an inexpensive, nonenzymic analytical system for prescreening substances that might cross-react as Rhus toxing (e.g., poison ivy, poison oak, and sumac allergens) on human skin. By spectrophotometric assay after incubation with an oxidizing mixture of Cu(II)ammine complex and ammonium persulfate, I could accurately and reproducibly determine o-quinoidal products of several potential synthetic cross-reactors and native poison ivy allergen, and could distinguish these from catecholamines, resorcinol, p-hydroquinone, and a closely related phenol. A good correlation was obtained between this nonenzymic technique and an enzymic assay. This Cu(II)ammine/persulfate oxidative assay, however, is inexpensive and obviates any spectral interference from enzymic proteins.