It is true that, when Langerhans cells migrate from the skin to the lymph node, they are transported via lymph vessels.

BACKGROUND: Generally, Langerhans cells deliver antigen information from the skin to the draining lymph nodes via lymph vessels. METHODS: By immunohistopathology, we investigated the delivery route of Langerhans cells in human skin using CD1a and S-100 protein antibodies. RESULTS: We noted CD1a- and S-100-positive Langerhans cells in the lymph vessels of the dermis. These were shaped like dendritic cells and presented with some lymphocytes, melanophages, melanin granules and lymph in the same vessels. CONCLUSION: These observations support the concept that Langerhans cells deliver antigen peptides to regional lymph nodes via afferent lymph vessels.

Antibacterial effect of beta-thujaplicin on staphylococci isolated from atopic dermatitis: relationship between changes in the number of viable bacterial cells and clinical improvement in an eczematous lesion of atopic dermatitis.

Beta-thujaplicin (hinokitiol) is a tropolone-related compound purified from the wood of Chamaecyparis obtusa, SIEB: et Zucc. and Thuja plicata D. Don. All Staphylococcus aureus isolates were inhibited by beta-thujaplicin with MICs of 1.56-3.13 mg/L. However, a paradoxical zone phenomenon occurred, with each isolate producing regrowth at higher beta-thujaplicin concentrations. Other antimicrobial agents showed a wide range of MICs. The combination of beta-thujaplicin and zinc oxide inhibited the paradoxical zone phenomenon, and enhanced killing activity against clinically isolated staphylococci. Large numbers of viable bacterial cells, especially S. aureus cells, were detected in the skin surface of atopic dermatitis, in comparison with those in healthy volunteers. The number of cells increased as the severity of the skin condition worsened. Topical application of beta-thujaplicin resulted in a reduction in the number of bacterial cells on the skin surface, and an improvement in skin condition after treatment. The results of this study suggest that the degree of reduction in the number of viable bacterial cells in an eczematous lesion of atopic dermatitis is related to the degree of improvement in skin condition.

Experimental study on phototoxicity and the photosensitization potential of ketoprofen, suprofen, tiaprofenic acid and benzophenone and the photocross-reactivity in guinea pigs.

BACKGROUND: Ketoprofen, suprofen and tiaprofenic acid are arylpropionic anti-inflammatories. Their chemical structures share the same elements as the benzoyl radical and the tiophene ring. We experienced nine cases of ketoprofen photoallergy, seven cases of suprofen photoallergy and three cases of tiaprofenic photoallergy. PURPOSE: To find the key structure of photosensitivity and photocross-reactivity to ketoprofen, suprofen and tiaprofenic acid. METHODS: : Three animals were tested for phototoxicity and six animals for the photosensitization potentials of ketoprofen, suprofen, tiaprofenic acid and benzophenone, and the photocross-reactivity of the above chemicals. Test substances were applied symmetrically on both sides of the animals' backs. The animals were irradiated with 180 mJ/cm2 UVB ((1/2) MED) and 10 J/cm2 UVA on the left side. The reactions were read on days 2, 3 and 4. The photosensitization potentials of ketoprofen, suprofen, tiaprofenic acid and benzophenone were determined using the Adjuvant-Strip method. Six animals were assigned to each test group and to a control group. RESULTS: Ketoprofen, suprofen, tiaprofenic acid and propionic acid showed negative reactions with the phototoxic test. Benzophenone showed phototoxic reactions to 40% acetone (ac.), 20% ac. and 10% ac. Therefore, we used 5% aq. benzophenone with the photosensitization test. Ketoprofen was the strongest photosensitizer (6/6) and showed photocross-reactivities to suprofen (2/6), tiaprofenic acid (3/6) and benzophenone (6/6). Suprofen was a strong photosensitizer (4/6) and showed photocross-reactivities to ketoprofen (1/4) and tiaprofenic acid (2/4), but not to benzophenone. Tiaprofenic acid was also a photosensitizer (2/6) but showed a photocross-reactivity only to benzophenone (2/2). Benzophenone was also the strongest photosensitizer (6/6), but did not photocross-react to the above three chemicals. CONCLUSION: From the test results, it appears that benzoyl radical is the key structure for photosensitivity and the photocross-reactivity of ketoprofen, suprofen and tiaprofenic acid. The whole structure of benzophenone was needed to induce photosensitization of benzophenone. The animals that were photosensitized from the entire structure of benzophenone did not photocross-react to ketoprofen, suprofen or tiaprofenic acid.

Contact urticaria due to polyethylene gloves.

We report a rare case of contact urticaria due to polyethylene gloves. The patient, a 46-year-old cook, had had had chronic urticaria since 1985, and first visited our hospital in June 2000. We began by prescribing antihistamine and antiallergenic drugs for him, but his condition did not improve. From a detailed interview, we established that when he put on polyethylene gloves at work, his condition worsened. We suspected some component of his gloves to be the cause of his symptoms. Prick and scratch tests with a solution extracted from his gloves showed a wheal-and-flare reaction at 15 min. We advised him to wear a cotton shirt under his clothes in daily life, and to put on cotton gloves under his polyethylene gloves while at work. Subsequently, the size and the number of wheals were markedly smaller and the subject's symptoms were reduced.

A case of contact urticaria syndrome due to di(2-ethylhexyl) phthalate (DOP) in work clothes.

We previously reported a case of contact urticaria syndrome (CUS) due to di(2-ethylhexyl) phthalate (DOP) in a polyvinyl chloride (PVC) grip on cotton gloves. The patient reported in this previous paper was careful not to have any contact with PVC products in his daily life or in his working environment. He discontinued the use of protective gloves with a PVC grip that was the cause of CUS. When working, he used cotton gloves without a PVC grip. We prescribed antihistamines which slightly improved his condition. However, when he wore work clothes while on duty, CUS relapsed. This condition was severe and made him feel anxious. When we advised him to wear a cotton shirt under his work clothes, the contact urticaria did not develop. We suspected that some component of the work clothes was the cause of his symptoms. A prick test with the extract solution of his work clothes showed a wheal and flare at the 15 min reading. The common component of the grip and the work clothes was found by analysis to be DOP.