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Notes: Cell adhesion molecules (CAMs) are cell surface glycoproteins expressed on several different cell lineages and involved in cell-cell and cell-matrix interactions in various physiological and pathological conditions.Numerous studies have shown that CAMs, a very substantial class of molecules subdivided into four families (integrins. the immunoglobulin-gene family, cudherins and lectin-like CAMs). are involved in the interaction of lymphocytes with keratinocytes, endothelial ceils and inter-and perivascular connective cells.Researchers have found a marked increase in the expression of CAMs with respect to normal skin in a variety of dermatoses, such as cutaneous necrotizing vasculitis. capillarities from unknown origin (purpura pigmentosa chronica). alopecia areata, lichen planus, systemic selerosis, psoriasis, etc. In the inflammatory and neoplastic skin diseases considered in this review, the adhesion molecules found to be chiefly expressed are ELAM-1, ICAM-I and LFA-I. This suggests that, predominantly, these adhesion molecules participate in the complex pathogenetic mechanisms conditioning the onset and development of these diseases. Knowledge of interaction mechanisms has led to identification of the role played by CAMs in the pathogenesis of these diseases and may represent a useful aid in the diagnosis and perhaps treatment of numerous skin pathologies.

Notes: Background. Alopecia areata (AA) is a noncicatricial alopecia with still unknown pathogenesis, but increasing evidence suggests that an immunologic process might be responsible for the disease. Materials and Methods. Nineteen patients with AA were studied with ten of them in the progressive phase of the disease and nine in the stabilized phase. Biopsies of both affected and unaffected skin were taken. For immunohistochemistry, monoclonal antibodies directed against CD3, CD4, CD8, CD10a, CD36, and HLA-DR antigens, were used, as well as antibodies directed against adhesion molecules icam-1, ELAM-1 and LFA-1. For electron microscopy (EM), specimens were fixed in glutaraldehyde-sodium cacodylate buffer, post-fixed in osmium tetroxide, and stained with uranyl acetate. For statistical analysis, sections from involved and uninvolved skin of each patient for each antibody, the sign test, Fisher's F-test, and the Tukey-Kramer test were used. Results. There was a rich infiltrate of CD4+ cells and CD1a+ cells, particularly in the perivascular zone of both unaffected and affected skin (here in the perivascular and in the peribulbar zone) in the progressive phase of AA. In the stabilized phase the infiltrate was scant, both in unaffected and affected skin and limited to the peribulbar area. Receptors of adhesion molecules (ICAM-2, ELAM-I, LFA-1) were strongly expressed, mainly at the microvascular level in both unaffected and affected skin in the progressive phase, but were only weakly or not at all expressed in the stabilized phase, again in unaffected and affected skin. Ultrastructural data confirmed the immunohistochemical findings and showed close contacts between infiltrating lymphocytes and Langerhans'-lineage cells mainly in the progressive phase. Conclusions. Our results suggest that: 1) an immunologic process, apparently carried out by CD4+ lymphocytes and by dendritic CD1a+ and CD36+ cells, may play a key role at least in the early phase of the disease involving primarily microvessels and later on the bulbar area; 2) the expression of adhesion molecule receptors is involved at the beginning of the disease by mediating the adherence of leukocytes to endothelial cells and subsequent trafficking into the dermis.

Notes: Background. In elderly individuals all components of the skin and subcutaneous tissue undergo histologic and ultra-structural changes. The turgidity of the dermis appears decreased, presumably due to altered patterns and levels of glycosaminoglycans (GAGS), especially hyaluronic acid and dermatan sulfate that are the most common. A linear, age-related decrease in the content of GAGS (mainly hyaluronic acid) has been hypothesized in human aged skin. Methods. We used the cationic dye Alcian Blue to selectively stain hyaluronic acid within the dermis in old and young subjects to compare ultrastructurally its topography and variations with age. Results. We demonstrated a progressive reduction in the number of electron-dense granules of hyaluronic acid and of their filaments until they were completely absent in subjects aged 60. Conclusions. We propose that the variations of the levels of hyaluronic acid in the dermis in aging could account for some of the most striking alterations of the aged skin, including decreased turgidity, less support for microvessles, wrinkling, and altered elasticity.

Notes: Background and Objective. The pathogenesis of leg ulcers due to chronic venous hypertension (CVH) seems to be related to perivenular fibrin-film formation due to decreased cutaneous fibrinolytic activity dependent on reduced release of tissue-type plasminogen activator that leads to tissue anoxia and ulcer formation. The purpose of the work is a spectrophotometric evaluation of urokinase (UPA) at the edge, the floor and in the periulcerous skin of leg ulcers. Methods. We examined a group of 10 patients with chronic leg ulcers caused by CVH. The biopsies from each patient were taken: (1) from the edge of the ulcer; (2) from the perilesional skin and (3) from the floor of the ulcer. Urokinase levels were evaluated in the same areas in 10 control subjects. The UPA activity was determined spectrophotometrically at 405 nm. Results. The results of our study showed that UPA is detectable in the center of the ulcer, on the edge, in the perilesional skin, as well as in the controls. Data are statistically significant. The highest levels of UPA are found at the edge of the ulcer; they were lower in the center and in the periulcerous skin. Conclusion. A chemoattracting effect of UPA on human keratinocytes has been documented and this study showed significantly higher levels of UPA at the edge and on the floor of the ulcers, suggesting a possible role of an UPA gradient that could promote mobilization of keratinocytes from the edge to the floor, thus inducing reepithelialization. Moreover, UPA could play some role in neoangiogenesis and fibroblast chemoattraction, thus contributing in various ways to wound healing.

Notes: Background. Progressive pigmented purpura (Schamberg's disease), a form of purpura pigmentosa chronica, is a lymphocytic capillaritis of unknown etiology and obscure pathogenesis. Our purpose was to assess the expression of cell membrane antigens (CD3, CD4, CD1a, CD36), of adhesion receptors (leukocyte function adhesion 1, LFA-1, endothelial leukocyte adhesion molecule 1, ELAM-1) intercellular adhesion molecule 1, ICAM-1), and the intercellular relationships in the early phase of the disease. Methods. Quantitative immunohistochemistry and electron-microscopy were performed on specimens of five subjects, aged 45 to 63 years. These studies were repeated in two patients after treatment with topical corticosteroid (betamethasone valerate cream 0.1%) and psoralen-ultraviolet A (puva). Results. The infiltrate consisted mainly of CD4+ lymphocytes and CD1a+ dendritic cells. Electron-microscopic investigation showed typical lymphocytes and two distinct types of dendritic cells. In the very early phase of the disease the adhesion receptors LFA-i and ICAM-1 were expressed intensely by all infiltrating cells; the adhesion receptors icam-1 and ELAM-i were expressed by endothelial cells. Close contact occured between lymphocytes and dendritic cells. After PUVA (120 J per cm2) and topical steroid therapy the infiltrate disappeared completely. Conclusions. These data suggest that a cell-mediated immune mechanism may be important in progressive pigmented purpura and that the early endothelial expression