muramidase and Erythema

Topics: Chemotactic Factors; Chemotaxis, Leukocyte; Cyclic AMP; Cyclic GMP; Dermatitis Herpetiformis; Erythema; Histamine Release; Humans; Immunoglobulin E; Muramidase; Neutrophils; Skin; Skin Diseases; Staphylococcal Infections

Damage to the skin extracellular matrix (ECM) is the hallmark of long-term exposure to solar UV radiation. The aim of our study was to investigate the changes induced in unexposed human skin in vivo after single or repeated (five times a week for 6 weeks) exposure to 1 minimal erythemal dose (MED) of UV solar-simulated radiation. Morphological and biochemical analyses were used to evaluate the structural ECM components and the balance between the degrading enzymes and their physiologic inhibitors. A three-fold increase in matrix metalloproteinase 2 messenger RNA (mRNA) (P < 0.02, unexposed versus exposed) was observed after both single and repeated exposures. Fibrillin 1 mRNA level was increased by chronic exposure (P < 0.02) and unaltered by a single MED. On the contrary, a single MED significantly enhanced mRNA levels of interleukin-1alpha (IL-1alpha), IL-1beta (P < 0.02) and plasminogen activator inhibitor-1 (P < 0.05). Immunohistochemistry demonstrated a significant decrease in Type-I procollagen localized just below the dermal-epidermal junction in both types of exposed sites. At the same location, the immunodetected tenascin was significantly enhanced, whereas a slight increase in Type-III procollagen deposits was also observed in chronically exposed areas. Although we were unable to observe any change in elastic fibers in chronically exposed buttock skin, a significant increase in lysozyme and alpha-1 antitrypsin deposits on these fibers was observed. These results demonstrate the existence of a differential regulation, after chronic exposure compared with an acute one, of some ECM components and inflammatory mediators.

Topics: Adult; alpha 1-Antitrypsin; Buttocks; Dose-Response Relationship, Radiation; Erythema; Extracellular Matrix; Extracellular Matrix Proteins; Gene Expression; Gene Expression Profiling; Humans; Interleukin-1; Matrix Metalloproteinase 2; Microscopy, Fluorescence; Muramidase; Peptide Fragments; Plasminogen Activator Inhibitor 1; Procollagen; RNA, Messenger; Skin; Sunlight; Ultraviolet Rays

We report on a patient with malignant histiocytosis (MH) presenting as multiple erythematous plaques and cutaneous depigmentation on her neck and chest. In a biopsy of an erythematous plaque, atypical large, foamy histiocytes infiltrated the dermis and positively stained with antibodies to lysozyme, leukocyte common antigen, and KP-1 (CD68). A few similar atypical cells were present in the superficial dermis focally in the depigmented areas. With use of immunohistochemical studies, most cases previously diagnosed as MH have been reclassified as T-cell lymphoma, B-cell lymphoma, or Ki-1-positive anaplastic large cell lymphoma. However, a few cases of "true" MH characterized by authentic histiocytes have been reported, presenting usually as red nodules. To our knowledge, our patient is the first with MH to present with erythematous plaques and vitiligo-like depigmentation.

Topics: Antigens, CD; Antigens, Differentiation, Myelomonocytic; Diagnosis, Differential; Erythema; Female; Histiocytic Sarcoma; Humans; Hypopigmentation; Leukocyte Common Antigens; Middle Aged; Muramidase; Skin Diseases; Skin Neoplasms

The skin is repeatedly exposed to solar UV radiation. Long-term photodamage is a consequence of cumulative UV radiation injury. Hence an examination of the repetitive effects of UV exposure is more likely to yield clues to the early alterations that lead to photoaged skin than a single exposure.. We examined the effects of repetitive low-dose UV irradiation on human skin with the aim of identifying UVA-induced effects that may have a different wavelength dependence than acute erythema.. Areas on the lower part of the back were each exposed to a suberythemal dose (0.5 minimal erythema dose [MED]) of solar simulated radiation (290 to 400 nm) and of UVA (320 to 400 nm) once daily, 5 days a week, for 28 doses. One site was also treated daily with a sunscreen having a sun protection factor of 22 and then exposed to 11 MEDs of solar simulated radiation for the same duration. Epidermal and dermal changes were analyzed and quantified by histochemical stains in combination with computer-assisted image analysis of tissue sections.. At equal 0.5 MED doses, UVA induced greater cumulative changes than solar simulated radiation, as assessed by development of a greater cumulative erythema response in the first week of treatment, the presence of epidermal hyperplasia and stratum corneum thickening, depletion of Langerhans cells, dermal inflammatory infiltrates, and deposition of lysozyme on elastin fibers. These changes were not prevented by the sunscreen. A single short-term dose of UVA did not elicit these changes.. These findings suggest that UVA may contribute significantly to long-term actinic damage and that the spectral dependence for cumulative damage does not parallel the action spectrum for acute injury (erythema) in human beings.

Topics: Adult; Biopsy; Epidermis; Erythema; Female; Histiocytes; Humans; Hyperplasia; Lymphocytes; Male; Mast Cells; Melanins; Muramidase; Radiation Dosage; Radiation Injuries; Skin; Sunscreening Agents; Time Factors; Ultraviolet Rays