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At least 109 records · Page 6Linked to original sources
PubMed2005

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.

Adolescent↗
PubMed1979

Studies on poison ivy. In vitro lymphocyte transformation by urushiol-protein conjugates.

The isolation and purification of poison ivy urushiol is described. The preparation of urushiol-ski protein and urushiol human serum albumin is also described. Lymphocytes from eleven donor naturally sensitized to poison ivy and from four non-sensitive individuals have been cultured for 5 days in the presence of urushiol-carrier conjugates. Lymphocytes from seven of the eleven sensitive donors responded with a stimulation index greater than 3.0 to urushiol-albumin conjugate. When urushiol-skin protein conjugate was used as a stimulant, lymphocytes from only three of the eleven sensitive donors responded. The results suggest that urushiol-protein conjugates can stimulate sensitive lymphocytes in vitro, although a response is not observed in every individual naturally sensitized to poison ivy.

Adult↗
PubMed1984

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.

Adolescent↗
PubMed1999

Putative skin-protective formulations in preventing and/or inhibiting experimentally-produced irritant and allergic contact dermatitis.

The effectiveness of skin protective formulations was evaluated in a previously-described in vivo human model. All formulations failed to inhibit ammonium hydroxide and urea irritation. Only paraffin wax in cetyl alcohol statistically (p<0.01) reduced Rhus allergic contact dermatitis. 3 commercial formulations markedly (p<0.001) suppressed sodium lauryl sulfate irritation. Paraffin wax in cetyl alcohol was quantitatively the most effective formulation. These results suggest that some formulations may provide protective effects against certain, but not all, irritants or allergens.

Adult↗
PubMed1996

In situ changes in the relative abundance of human epidermal cytokine messenger RNA levels following exposure to the poison ivy/oak contact allergen urushiol.

Abstract: Epidermal keratinocytes in culture have been shown to produce many cytokines, and their proteins have been identified in skin tissue samples. It has therefore been assumed that these cytokines are transcribed in vivo by the epidermis in response to contact allergens. 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. In sensitive subjects, IL-1 alpha and TNF-alpha mRNAs showed a progressive increase in transcript levels that paralleled the clinical and histological features of the inflammatory process. The time-course of the IL-1 beta response differed from that of IL-1 alpha and TNF-alpha, in that there was an early (by 6 h after urushiol administration) elevation in IL-1 beta mRNA that occurred before there was evidence of inflammation and had returned to background levels by 72 h when the reaction had reached its peak. In contrast to urushiol-sensitive subjects, urushiol-anergic individuals did not exhibit an increase in IL-1 alpha, IL-1 beta or TNF-alpha mRNA levels. The data provide evidence for an in vivo role for epidermal IL-1 alpha, IL-1 beta and TNF-alpha transcription in the regulation of IL-1 beta and TNF-alpha polypeptide levels in the epidermis in response to this common contact allergen.

Adult↗
PubMed1965

Basophil degranulation induced by oral poison ivy antigen.

Seven subjects shown by patch test to be sensitive to poison ivy oleoresin were challenged with graded oral doses of ivy extract. In each instance the circulating basophil leukocytes showed significant degranulation within one hour of challenge. This finding was interpreted as evidence of the presence of immediate-type circulating antibody to ivy antigen in these subjects. No drop in the absolute basophil count was noted, but with higher oral doses the degranulation persisted for several days. Thirteen control subjects showed no change in the basophil morphology or count, indicating that the resin at these levels was not toxic to this cell. All but one of the sensitive subjects showed objective patch test evidence of hyposensitization following the intensive three-week course of oral poison ivy antigen.

Antigens↗
PubMed1975

Renal lesions accompanying poison oak dermatitis.

Renal damage associated with poison oak dermatitis is extremely rare in humans after exposure to urushiol antigen. Three renal lesions have been described: proliferative glomerulonephritis, arteritis, and membranous nephropathy. The present study reports on three patients who developed nephropathy after exposure to poison oak. One patient was studied by renal biopsy (including electron microscopy and immunofluorescence techniques) and another by autopsy findings. One of these patients had a typical membranous nephropathy, the other, proliferative glomerulonephritis with necrotizing arteritis and glomerulitis. In the patient with membranous nephropathy antibody to urushiol was discovered by passive cutaneous anaphylaxis in the guinea pig.

Animals↗