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Biomedical subjects

I Ghersetich

Publications and source records attributed to I Ghersetich.

At least 19 recordsLinked to original sources
PubMed1996

Alopecia areata: immunohistochemistry and ultrastructure of infiltrate and identification of adhesion molecule receptors.

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-1, 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.

Adolescent↗
PubMed1995

Cell infiltrate in progressive pigmented purpura (Schamberg's disease): immunophenotype, adhesion receptors, and intercellular relationships.

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-1 and ICAM-1 were expressed intensely by all infiltrating cells; the adhesion receptors ICAM-1 and ELAM-1 were expressed by endothelial cells. Close contact occurred 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 of adhesion receptors may determine the pattern of organization of the pericapillary infiltrate.

Administration, Topical↗
PubMed1995

Working classification of vasculitis.

Vasculitis is defined as angiocentric segmental inflammation of the blood vessels and fibrinoid necrosis of the vessel wall. Classification of vasculitis is a controversial problem, because of the difficulty in incorporating globally different criteria such as histologic features, size of affected blood vessels, etiology, pathogenesis and other factors in a single classification schema. In this paper we review the principal classifications and make a novel attempt to classify vasculitis on the basis of the size of affected vessels. We hope that a new generation of basic and clinical investigators can achieve a better understanding of the pathogenesis of various vasculitis-related syndromes and that this understanding will facilitate future classification schemas.

Humans↗
PubMed1995

Cellular steps in the pathogenesis of cutaneous necrotizing vasculitis.

Cutaneous necrotizing vasculitis (CNV) have been traditionally divided into "leukocytoclastic" and "lymphomonocytic" forms. The etiology and the pathogenesis of the two forms are not clear. We studied by immunohistochemistry and electronmicroscopy the infiltrate of 5 cases of leukocytoclastic form and 5 cases of lymphomonocytic form of CNV in two phases (early and late). Aim of the study was to evaluate: 1. the immunophenotypical characteristics of the infiltrate; 2. the expression of some adhesion molecules receptors; 3. the ultrastructural characteristic of the infiltrate; 4. the possible sequence of the events. Our results showed, by immunohistochemistry, a rich infiltrate of CD3+, CD4+, CD1a+ cells in both phases of lympho-monocytic vasculitis and a poor infiltrate of CD4+, CD1a+ and CD36+ cells in the early phase of leukocytoclastic vasculitis, while the perivascular infiltrate was rich of these cells in the late phase of this latter form. ICAM-1 and LFA-1 were strongly expressed in lympho-monocytic vasculitis. By electronmicroscopy, most infiltrating cells showing the ultrastructural markers of immature cells of dendritic lineage were in contact with each other and with lymphocytes and perivascular dendritic macrophages in lymphocytic form and in the late phase of leukocytoclastic form. Our results suggest that lymphocytic vasculitis might be related to a cell-mediated immune reaction and that the leukocytoclastic form of CNV, formerly considered a typical neutrophilic disease, is also maintained by a cell-mediated immune response to not yet identified endogenous antigens released in the lesional area.

Adult↗
PubMed1995

Langerhans cells and vasculitis.

Langerhans cells are members of the dendritic cell system, which reside in the skin. These cells have many immunohistochemical and ultrastructural markers (for example, they are CD1a+ and possess Birbeck granules), which consent to identify them in an infiltrate. Langerhans cells have the specific role to present the antigens to T lymphocytes and to induce the cell-mediated immune reaction. Cutaneous necrotizing vasculitis (CNV) can be divided in two major forms: a leukocytoclastic type and a lymphocytic type. The pathogenesis of the first one is presumably immune complex-mediated, while for the second one a cell-mediated immunity has been proposed. Our group investigated on the cell infiltrate of some cases of CNV, both leukocytoclastic and lymphocytic type; and for leukocytoclastic CNV two phases were studied: an early one (at the onset of the lesion) and a later one (more than 24 hours). Special attention was paid to the presence of dendritic cells in the infiltrate and to their relationship to lymphocytes, if present. By immunohistochemistry and electron microscopy we could find many Langerhans cells and T lymphocytes in lymphocytic and in the late phase of leukocytoclastic CNV. The observed pattern of the cell infiltrate suggests that a cell mediated immune response play a major role in the pathogenesis of lymphocytic vasculitis and that dendritic cells and lymphocytes contribute to self-perpetuate leukocytoclastic vasculitis, which cannot be anymore considered as simply due to infiltration of neutrophils.

Animals↗
PubMed1995

Gamma/delta T lymphocytes in cutaneous necrotizing vasculitis.

Sections of lesional skin of 5 patients with leukocytoclastic cutaneous necrotizing vasculitis (CNV) (3 with documented infective etiology and 2 with unknow etiology) and of 5 patients with lymphocytic CNV with unknow etiology were investigated with immunoperoxidase technique. In lymphocytic CNV the dermal infiltrate was mainly constituted of CD3+, CD4+, CD1a+ and CD36+ cells. ICAM-1 and LFA-1 were strongly expressed. In leukocytoclastic CNV the infiltrate was poor of these cells in the early phase of disease, but they increased in the late phase. ICAM-1 and LFA-1 were strongly expressed in the late phase, while gamma/delta T cells and the expression of 72 kD heat shock protein were significantly present only in leukocytoclastic CNV with documented infective etiology. These results seem to suggest the role of a secondary cell-mediated immune response in the late phase of leukocytoclastic CNV, indicating gamma/delta T cells as a possible clue to the infective etiology of CNV.

Adult↗
PubMed1994

Hyaluronic acid in cutaneous intrinsic aging.

BACKGROUND: In elderly individuals all components of the skin and subcutaneous tissue undergo histologic and ultrastructural 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 Alcain 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 microvessels, wrinkling, and altered elasticity.

Adult↗
PubMed1994

Ultrastructural study of hyaluronic acid before and after the use of a pulsed electromagnetic field, electrorydesis, in the treatment of wrinkles.

BACKGROUND: Treatment of wrinkles has become an increasing problem for dermatologists. Hyaluronic acid is a component of the family of glycosaminoglycans (GAGS, substances known for their property of retaining water), that significantly decreases with aging and in wrinkles. A new technique that uses a specific pulsed electromagnetic field, electrorydesis, has been introduced in the treatment of wrinkles associated with aging. The treatment is based on the reported in vitro effects of specific electromagnetic fields on fibroblast cultures (e.g., an increase in DNA synthesis and in the production of collagen and presumably also of GAGS). METHODS: The in vivo effects of the electromagnetic field on aged skin (3 subjects aged 50, 56 and 60 years), with particular focus on the ultrastructural modifications and GAGS amount before and after the treatment, were evaluated by electron microscope. RESULTS: The ultrastructural study (tissue stained with alcian blue) showed after treatment a significant increase (p < 0.005) of the electron-dense granules (corresponding to hyaluronic acid), located in collagen elastic fibers, and in the soluble matrix. This presumably leads to subsequent edema that was clinically evident after the treatment. CONCLUSIONS: These data suggest that the increased levels of GAGS and the subsequent edema of the dermis could explain at least in part the clinical changes observed after electrorydesis treatment (e.g., swelling and "disappearance" of the wrinkle).

Electromagnetic Fields↗
PubMed1994

alpha-Interferon cream restores decreased levels of Langerhans/indeterminate (CD1a+) cells in aged and PUVA-treated skin.

Langerhans/indeterminate (CD1a+) cells are known for their role in stimulating T-lymphocyte-dependent immune reactions. They are normally present in the skin and are modified in a variety of different pathological and physiological events, including aging. Linear decrease of CD1a+ cells with aging (both true aging and photoaging) is considered the most important cause of reduced immunosurveillance in aged old skin of the elderly. Recently it has been suggested that alpha-interferon might have an effect on increasing levels of dendritic cells in aged and photoaged skin. We studied biopsies from the preauricular area in 15 subjects (5 subjects aged 18-21 years, 5 aged 57-75, and 5 aged 30-45 who underwent PUVA therapy, total irradiation 120 J/cm2) before and after the application of alpha-interferon cream. Our findings show that dendritic cells are significantly decreased in the 57- to 75-year-old group compared to the 8- to 21-year-old group. After PUVA therapy we also found a decrease in Langerhans cells. Our study shows that the application of alpha-interferon cream induces an increase in cutaneous CD1a+ cells and HLA-DR+ cells in both older subjects and subjects who have undergone PUVA therapy. On the basis of these results, one could hypothesize that alpha-interferon cream may have some beneficial effects on photoaging-reduced immunosurveillance.

Administration, Topical↗
PubMed1994

Treatment of psoriasis vulgaris with topical calcipotriol: is the clinical improvement of lesional skin related to a down-regulation of some cell adhesion molecules?

Calcipotriol is demonstrably efficacious for the treatment of psoriasis by virtue of its effects on the skin's immune system and on epidermal growth. We performed this study to emphasize the difference in the expression of certain cell adhesion molecules (CAMs) (ICAM-1, ELAM-1, LFA-1, VLA-3, VLA-6) in lesional and perilesional skin of 10 patients with psoriasis, before and after treatment with topical Calcipotriol. We took two biopsies of lesional and perilesional skin from each patient before and after treatment and then performed an immunohistochemical study to observe the expression of these CAMs, utilizing monoclonal antibodies against these adhesion molecules. We noticed reduced levels of infiltrating cells along with the expression of ICAM-1, LFA-1, ELAM-1 and of CAMs VLA-3, VLA-6 in basal and suprabasal keratinocytes. On the basis of these data we hypothesize that, besides epidermal keratinocytes, another target for Calcipotriol may be the skin's own immune system, suggesting that Calcipotriol can modify T lymphocyte activity (IL-1 dependent) through a down-regulation of CAMs.

Administration, Topical↗
PubMed1993

Mesoglycan treatment restores defective fibrinolytic potential in cutaneous necrotizing venulitis.

BACKGROUND: Cutaneous necrotizing venulitis (CNV) is a clinical disorder associated with segmental inflammation and fibrinoid necrosis of the dermal venules. It usually presents clinically as palpable purpura, even sometimes as nodules, bullae, ulcers, and urticarial lesions. This form, when showing as leukocytoclastic vasculitis is apparently characterized by the tissue deposition of circulating immune complexes and by reduced cutaneous (CFA) and plasma (PFA) fibrinolytic activity due to reduced release of plasminogen activator (PA) from the venular endotheliocytes. Reduced CFA and PFA cause large amounts of fibrin deposits in both intra- and perivascular areas, which are able to magnify and self perpetuate the inflammatory processes following immune complex deposition. METHODS: We have studied both the PFA and CFA potential (the maximum amount of PA released in the skin after certain stimuli) and the deposits of immunoglobulins, C3, and fibrin related antigen, before and after intradermal injection of histamine (a substance able to provoke endothelial release of PA), in three subjects affected by CNV before and 20 days after 10 mg/kg/day I.M. treatment with the fibrinolytic agent mesoglycan. RESULTS: Cutaneous fibrinolytic activity and CFA potential, reduced prior to treatment, was normal after treatment, while the deposits of immunoglobulins (IgA, IgG and IgM), C3, and fibrin related antigen, detected with direct immune fluorescence (DIF) showed similar findings before and after treatment. CONCLUSIONS: These data suggest that reduced CFA may play a major role in the pathogenesis of the immunologically mediated injury in CNV. The intraperivascular deposition of fibrin is favored. The fibrinolytic agent mesoglycan seems effective in restoring defective fibrinolysis in patients affected by cutaneous necrotizing venulitis, suggesting that in cases with reduced cutaneous fibrinolytic activity (or potential) the use of a fibrinolytic agent should be considered.

Adult↗
PubMed1990

Proteoglycans in so-called cellulite.

Glycosaminoglycans are a group of polysaccharide chains covalently linked to proteins to form proteoglycan molecules with high water-attracting properties. The ultrastructural localization of glycosaminoglycans in the so-called cellulite skin and in normal subjects was studied. Data show that there is increasing concentration of glycosaminoglycans in the cellulite skin, presumably leading to a rise in the amount of water retained in the skin in this disease.

Adipose Tissue↗