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Biomedical subjects

A España

Publications and source records attributed to A España.

At least 37 records · Page 2Linked to original sources
PubMed1997

Differential modulation of IL-8 and TNF-alpha expression in human keratinocytes by buflomedil chlorhydrate and pentoxifylline.

Pentoxifylline (PTX) is a methylxanthine derivative used in a wide range of dermatoses. As well as its hemorrheologic activity, PTX has anti-inflammatory properties. Buflomedil chlorhydrate (BC) is another hemorrheological drug with peripheral vasodilatory action, whose clinical uses are similar to those of PTX. Both drugs increase intracellular levels of cAMP, either secondary to phosphodiesterase inhibition (PTX) or adenyl-cyclase stimulation (BC). Long-term cultures of normal human keratinocytes were prepared in a free-serum medium, and stimulated with 1 mg/ml of phorbol 12-myristate 13-acetate (TPA) and PTX or BC (100-1000 micrograms/ml). Levels of TNF-alpha, IL-1 alpha, IL-1 beta, IL-8 and TGF-beta 1 using ELISA and Northern blot or RT-PCR techniques were measured. TPA-induced TNF-alpha and IL-8 release from keratinocytes. TPA did not induce IL-1 alpha or IL-1 beta release of keratinocytes. TPA increased RNA expression of the TNF-alpha, IL-1 alpha, IL-1 beta, IL-8 and TGF-beta 1. BC diminished TPA-induced TNF-alpha and IL-8 release from keratinocytes; in the case of IL-8 it is possible that this inhibition occur to transcriptional level. Moreover PTX was unable to inhibit TNF-alpha and IL-8 synthesis and expression. PTX and BC reduced TPA-induced IL-1 alpha and beta expression. It is possible that BC action is specifically exerted on keratinocytes, because we did not find similar results with TNF-alpha and IL-8 synthesis in mononuclear peripheral blood cells.

Cells, Cultured↗
PubMed1997

The desmosome and hemidesmosome in cutaneous autoimmunity.

Epidermal blister formation is the hallmark of three cutaneous autoimmune diseases: pemphigus foliaceous (PF), pemphigus vulgaris (PV) and bullous pemphigoid (BP). In PF and PV, blistering is due to acantholysis (cell-cell detachment) in the subcorneal and suprabasal epidermal layers, respectively, while BP is characterized by detachment of the basal epidermal cells from the underlying dermis. For several years, we have focused our research efforts on elucidating the pathogenic mechanisms operating in these bullous diseases. Early studies performed by our research group and others revealed that in all three diseases, the patients produce autoantibodies that bind to target antigens located on the surface of cells that are undergoing detachment. Thus it was hypothesized that these anti-epidermal autoantibodies played a role in initiating blister formation. We recognized that elucidating the normal mechanisms of epidermal cell-cell and cell-dermis adhesion would help us understand the abnormal epidermal cell detachment seen in these patients. We hypothesized that under normal conditions these adhesive mechanisms in the epidermis are complex and dynamic and mediated by the interaction of cell surface molecules unique to each layer of the epidermis. Also, we postulated that PV, PF and BP autoantibodies may cause cell detachment by impairing the function of their respective epidermal cell surfaces. Support for this hypothesis has come from recent studies which showed that PV and PF autoantibodies recognize distinct, yet related, desmosomal glycoproteins in the cadherin family of calcium-dependent adhesion molecules. The epidermal antigen in PV is desmoglein-3 (dsg3), while in PF it is desmoglein-1 (dsg1). These anti-epidermal autoantibodies have been shown to be pathogenic in passive transfer experiments. Neonatal mice injected with these antibodies develop intraepidermal blisters characteristic of the corresponding human disease. Autoantibodies in BP react with BP180 and BP230, two major components of the hemidesmosome, a cell structure involved in dermal-epidermal adhesion. Recent passive transfer mouse model studies performed in our laboratory have shown that anti-BP180 antibodies can induce subepidermal blistering in the experimental animals. Moreover, the pathogenic mechanism was shown to be dependent on complement activation and recruitment of neutrophils to the dermal-epidermal junction. In conclusion, desmosomal glycoproteins are the targets of autoimmune injury in PV and PF. The anti-epidermal autoantibodies may cause intraepidermal blisters by impairing the function of dsg1 and dsg3. In BP the hemidesmosome is the target. It appears that antiBP180 antibodies cause subepidermal blister formation by triggering a complement- and neutrophil-mediated inflammatory process.

Animals↗
PubMed1996

Photo-induced toxic epidermal necrolysis caused by clobazam.

Toxic epidermal necrolysis (TEN) is a life-threatening disease, the pathogenesis of which remains largely unknown. We describe a 23-year-old woman under treatment with clobazam who developed lesions of TEN in light-exposed areas. Patch and photopatch tests with clobazam were negative. The cellular phenotype and cytokines were studied in blister fluid. The cellular infiltrate was composed mainly of T lymphocytes with a predominant cytotoxic phenotype. There was an increase in the level of tumour necrosis factor (TNF)-alpha in blister fluid compared with the control (a patient with bullous pemphigoid).

Adult↗
PubMed1996

Effects of low concentrations of cis- and trans-urocanic acid on cytokine elaboration by keratinocytes.

The urocanic acid cis isomer (cis-UCA) is a possible cutaneous photoreceptor for the immunomodulatory phenomena that follow ultraviolet B irradiation. Several experiments in animals show an inhibitory action of cis-UCA on cellular immunity. However, the action of cis-UCA on the synthesis of cytokines in keratinocytes remains unknown. Long-term cultures of normal human keratiocytes were prepared in a serum-free medium, and stimulated with 1 microgram/ml of phorbol 12-myristate 13-acetate (TPA) and UCA or UVB-UCA (10-100 micrograms/ml). Synthesis of the following cytokines was measured using ELISA and Northern blot techniques: TNF-alpha, IL-1 alpha, IL-1 beta, IL-6, IL-8 and TGF-beta 1. TPA increased TNF-alpha protein levels in culture supernatants. No changes in Il-1 alpha and IL-1 beta protein levels were detected in basal culture supernatant after TPA stimulus. TPA augmented RNA expression for TNF-alpha, IL-1 alpha, IL-1 beta and TGF-beta 1. UCA isomers did not induce cytokine changes in protein synthesis. Expression of IL-1 alpha and IL-1 beta genes was increased after exposure to 100 micrograms/ml UVB-UCA (70 micrograms/ml cis-UCA). A slight increase in TNF-alpha RNA expression was detected when the dose of UVB-UCA reached 100 micrograms/ml. No effects on cytokine synthesis were found after UCA stimulus. These results suggest that low doses of cis-UCA do not effect cytokine synthesis by keratinocytes.

Breast↗
PubMed1995

Skin cancer in heart transplant recipients.

BACKGROUND: The frequency of skin cancer in organ transplant recipients is high, up to 15%. OBJECTIVE: Our purpose was to determine the incidence of skin cancer in patients who underwent immunosuppression after heart transplantation and to determine the factors important in the appearance of skin cancer. METHODS: We studied the frequency of skin cancer in 92 of 111 patients after they underwent heart transplantation between January 1984 and December 1993. RESULTS: At least one cutaneous neoplasm (squamous cell carcinoma and/or basal cell carcinoma) developed in 14 patients (15.2%). The basal cell carcinoma to squamous cell carcinoma ratio was 1:1.5. The skin cancer appeared an average of 31.5 months after transplantation; the average was 36 months for squamous cell carcinoma and 25.3 months for basal cell carcinoma. Cumulative risk rose from 4.3% at 1 year up to 43.8% at 7 years after transplantation. The overall incidence of both types of skin cancer was 45.3 per 1000 posttransplant person-years, with an incidence of 25.8 for basal cell carcinoma and 29.1 for squamous cell carcinoma. Most skin cancers developed between 2 and 3 years after transplantation. All patients were exposed to a significant amount of ultraviolet radiation and had skin type II or III. We did not find a significant association between skin cancer and haplotype HLA-A3, HLA-A11, HLA-DR, and the number of mismatches for HLA-B. CONCLUSION: We found an increased progressive cumulative incidence of skin cancer in heart transplant recipients for two reasons: (1) immunosuppression and increased exposure to ultraviolet radiation in some patients, and (2) the skin type of certain patients. We emphasize the need for photoprotection in this group of patients and regular skin cancer screening examinations.

Adult↗
PubMed1995

Transfusion-associated acute graft-versus-host disease in a heart transplant recipient.

We report a heart transplant recipient who developed graft-versus-host disease (GVHD) following blood transfusion. We consider that heart transplant recipients should be included in the category of immunosuppressed patients who may develop this disease after being treated with blood products. We also consider that, at the present time, irradiation of blood products is the only useful method of avoiding development of GVHD in these patients.

Female↗
PubMed1994

Generalized skin reaction following tinea pedis (dermatophytids).

An 11-year-old boy presented with inflamed tinea pedis followed by a generalized id type skin eruption, with disappearance of the rash after treatment of the mycotic foot lesions. The pathogenesis of this process is not precisely known. Fungal infection was not detected from the generalized skin lesions. Various clinical forms of dermatophytid reaction are discussed.

Child↗
PubMed1993

Graft-versus-host disease after liver transplantation.

We describe a case of graft-versus-host disease that developed in the recipient of an orthotopic liver transplant. A maculopapular eruption developed on postoperative day 25. After the diagnosis of graft-versus-host disease was made aggressive therapy was instituted, which resulted in a complete recovery.

Exanthema↗