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W Czech

Publications and source records attributed to W Czech.

At least 37 records · Page 2Linked to original sources
PubMed1996

Soluble E-selectin in sera of patients with atopic dermatitis and psoriasis--correlation with disease activity.

E-selectin endothelial leucocyte adhesion molecule-1 is expressed on endothelial cells in distinct inflammatory skin diseases. E-selectin mediates the adhesion between activated endothelium and different inflammatory cells. To evaluate soluble E-selectin as a marker of disease activity in patients with atopic dermatitis and psoriasis, the concentration of soluble E-selectin, determined by ELISA, was studied in sera of patients before and after treatment and compared with normal non-atopic controls. The disease severity was established using clinical scoring systems. Levels of soluble E-selectin were significantly elevated in sera of patients with atopic dermatitis and psoriasis (as compared with controls). Clinical improvement, after treatment, in patients with atopic dermatitis, but not in psoriasis, was associated with a significant decrease in serum levels of soluble E-selectin. There was a significant correlation of soluble E-selectin and disease activity in patients with atopic dermatitis. These data indicate that soluble E-selectin is another parameter to evaluate the inflammatory response in atopic dermatitis and psoriasis. Determination of soluble E-selectin may be a useful measure of disease activity in atopic dermatitis.

Adolescent↗
PubMed1996

Modulation of intercellular adhesion molecule 1 (ICAM-1) expression on the human mast-cell line (HMC)-1 by inflammatory mediators.

The effect of inflammatory mediators on the expression of several surface adhesion molecules on the human mast-cell line (HMC)-1 was studied. By flow cytometry, it could be shown that among several surface adhesion molecules (ICAM-1/CD54, VLA-4/CD49d, Mac-1/CD11b, LFA-1/CD11a, LFA-2/CD2, LFA-3/CD58, VCAM-1), only the constitutively expressed immunoglobulin family member intercellular adhesion molecule-1 (ICAM-1) is modulated by proinflammatory cytokines on HMC-1 mast cells. Stimulation with tumor necrosis factor-a (TNF-alpha) and interferon-gamma (IFN-gamma) resulted, in addition to interleukin-(IL-)4, in selective upregulation of ICAM-1 expression. Costimulation of either IL-4 or IFN-gamma with TNF-alpha further increased the ICAM-1 expression as compared to the stimuli alone. In contrast, stem-cell factor (SCF), granulocyte/macrophage colony-stimulating factor (GM-CSF), IL-10, IL-8, monocyte chemotactic and activating factor (MCAF), and the complement split product C5a failed to modulate the expression of any adhesion molecule examined. The levels of cytoplasmic free calcium in HMC-1 mast cells were not altered by cross-linking surface ICAM-1, suggesting linkage of other intracellular signaling pathways. This cytokine-induced upregulation of ICAM-1 expression might reveal a putative regulatory mechanism of mast-cell interaction with effector cells bearing the counterparts of ICAM-1 (CD54), the molecules Mac-1 (CD11b/CD18) and leukosialin (CD43), and the principal ligand LFA-1 (CD11a/CD18).

Cytokines↗
PubMed1995

Release of sulfidoleukotrienes in vitro: its relevance in the diagnosis of pseudoallergy to acetylsalicylic acid.

Pseudo-allergic reactions (PAR) are caused by a variety of drugs, of particular interest by acetylsalicylic acid (ASA) and other nonsteroidal antiinflammatory drugs. The clinical symptoms often resemble immediate type hypersensitivity reactions and consist of bronchospasm, urticaria, angioedema and even anaphylactic shock. Antigen specific immune mechanisms, however, are not involved. In general, skin tests are not reliable and the diagnosis of PAR is based mainly on risky provocation tests. Therefore, the purpose of this study was to establish procedures for in vitro diagnosis of PAR to ASA. A controlled study was performed including patients with PAR to ASA based on history and positive oral provocation test and non-atopic as well as atopic controls. In this in vitro study the production of sulfidoleukotrienes (sLT) by isolated leukocytes was measured by cellular allergen stimulation test (CAST), which is based on detection of LTC4, LTD4 and LTE4 by a monoclonal antibody. Accordingly, the direct effect of ASA as well as the modulatory effect of ASA on C5a-induced production of sLT in leukocytes in vitro was investigated. In patients with PAR to ASA, C5a-induced generation of sLT was significantly increased as compared to normal controls. In contrast, there was no difference in the spontaneous release of sLT in vitro in patients and controls. Preincubation of leukocytes with ASA did not exert a significant modulatory effect on the spontaneous or the C5a-induced production of sLT in patients and controls. In summary, the present study provides a novel in vitro test system for the diagnosis of PAR to ASA by measurement of sLT release in leukocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Analysis of the cytokine pattern expressed in situ in inhalant allergen patch test reactions of atopic dermatitis patients.

In the present study, we examined the cytokine pattern expressed in situ during the development of eczematous reactions that had been provoked in atopic dermatitis patients by patch testing with house dust mite allergen. In 24-h house dust mite allergen patch test reactions, expression of interleukin (IL)-4 mRNA and IL-2 mRNA increased, but interferon (IFN)-gamma mRNA did not, as compared with control skin. In 48-h inhalant allergen patch test reactions, however, IFN-gamma mRNA and IL-2 mRNA expression were increased above levels observed in control skin, whereas IL-4 mRNA expression was decreased below background levels. These data demonstrate that a switch from a Th2-like to a Th1-like cytokine response occurs in inhalant allergen patch tests of atopic dermatitis patients. This biphasic pattern was specific to inhalant allergen patch test reactions, as it was not observed in irritant reactions in the same patient. IFN-gamma production by T cells may be induced by the cytokine IL-12. In the present study, up-regulation of IFN-gamma mRNA expression in inhalant allergen patch test reactions was preceded by an increased expression of the p35 subunit of IL-12 mRNA. These observations suggest that increased IL-12 expression may contribute to the observed switch of the in situ cytokine secretion pattern. Further studies are necessary to determine whether a similar biphasic pattern of cytokine expression is also operative in the initiation phase of atopic eczema.

Allergens↗
PubMed1995

IgE autoantibodies in atopic dermatitis--occurrence of different antibodies against the CH3 and the CH4 epitopes of IgE.

Levels of "free" anti-IgE autoantibodies and IgE/anti-IgE immune complexes were measured in the sera of patients with atopic dermatitis before and after treatment, psoriasis patients, and nonatopic controls. In this measurement, we used two monoclonal antibodies with distinct in vitro functions (LE 27, BSW 17), directed against the epsilon CH3 and CH4 domains of the IgE Fc-fragment, in a novel immunobinding assay. In patients with atopic dermatitis, elevated levels of "free" anti-IgE antibodies and IgE/anti-IgE immune complexes were detected in comparison to psoriasis patients and controls. In addition, there was a positive correlation between total IgE and the amount of IgE/anti-IgE complexes detected by LE 27 (r = 0.7; P < 0.001) or BSW 17 (r = 0.64; P < 0.001) in patients with atopic dermatitis. In contrast, an inverse correlation was observed between total IgE and "free" anti-IgE antibodies (r = -0.34; P < or = 0.05) in atopic dermatitis. However, serum levels of anti-IgE autoantibodies before and after therapy in patients with atopic dermatitis did not differ, and levels of anti-IgE antibodies did not correlate with clinical severity, as evaluated by an established clinical scoring system. Our data clearly indicate that significantly elevated amounts of anti-IgE antibodies could be observed in patients with atopic dermatitis, which are directed against different epitopes on the IgE molecule. It is tempting to speculate that these autoantibodies exert different effects of IgE-receptor-bearing effector cells and may play an important role in IgE regulation.

Adolescent↗
PubMed1994

C3a activates the respiratory burst in human polymorphonuclear neutrophilic leukocytes via pertussis toxin-sensitive G-proteins.

In contrast to C5a, which represents a well-established potent activator of the respiratory burst in polymorphonuclear neutrophilic granulocytes (PMN), the functional role of C3a in the activation of PMN is, so far, poorly understood. Herein, the potential role of human C3a in the activation of the respiratory burst in human PMN was investigated. The release of reactive oxygen species (ROS) of PMN from healthy donors was measured by lucigenin-dependent chemiluminescence. C3a dose-dependently induced the production of ROS in human PMN in the range between 10 ng/mL and 1,000 ng/mL, whereas C3a-desArg was inactive. Flow cytometric measurement of H2O2 by dihydrorhodamine-123 labeling of anti-CD16-stained PMN showed that predominantly neutrophilic PMN are responsible for the C3a-induced activation of the respiratory burst. To exclude that C3a stimulation was caused by contamination with C5a, the specificity of C3a-induced activation of PMN was shown using monoclonal antibodies (MoAbs). Accordingly, the effect of C3a was completely abolished in the presence of Fab fragments of a blocking anti-C3a MoAb. In addition, blockade of the C5a receptor by the anti-C5a receptor (anti-C5aR) MoAb, S5/1, totally inhibited the C5a-induced production of ROS, whereas the C3a response in the presence of the anti-C5aR MoAb was unaffected. The specificity of the response was further confirmed by homologous desensitization after restimulation with C3a. In contrast, no cross-desensitization was observed upon stimulation with C5a. The C3a-induced ROS production by PMN was inhibited by pertussis toxin, indicating the involvement of guanine nucleotide-binding proteins (Gi proteins) in the signal transduction process initiated by C3a. In addition, stimulation of PMN by C3a resulted in a transient increase in the cytosolic free calcium concentration ([Ca2+]i) in a dose-dependent manner. In contrast to C3a-induced ROS production, C3a did not induce a chemotactic response in PMN, indicating functional qualitative differences as compared with C5a. In summary, these results show that C3a is a potent activator of the respiratory burst in human PMN. Therefore, these findings point to a novel role of C3a in the pathogenesis of inflammatory diseases associated with increased C3a levels and PMN activation.

Calcium↗
PubMed1994

C3a activates reactive oxygen radical species production and intracellular calcium transients in human eosinophils.

Whereas C5a is a well-established potent activator of eosinophils, the functional role of C3a in the activation of eosinophils is, so far, poorly understood. Here, the activation of human eosinophils stimulated with C3a was analyzed and compared to C5a activation. Flow-cytometrical measurements revealed that stimulation of eosinophils by C3a resulted in a transient elevation of the intracellular calcium concentration ([Ca2+]i) in a dose-dependent manner. In addition, the production of reactive oxygen radical species (ROS) of eosinophils after C3a and C5a stimulation was measured by lucigenin-dependent chemiluminescence and quantified by superoxide dismutase-inhibitable reduction of ferricytochrome C. Half maximal and maximal ROS production in response to C3a was observed at 50 ng/ml and 1000 ng/ml, respectively, whereas C3a-desArg was inactive. To ensure that C3a stimulation was not caused by contamination with C5a, monoclonal antibodies were used to demonstrate the specificity of C3a. The effect of C3a was completely abolished in the presence of monovalent antigen-binding fragments of a functionally blocking anti-C3a monoclonal antibody. In addition, blockade of the C5a receptor by the monoclonal anti-C5a receptor antibody S5/1 totally inhibited the C5a-evoked ROS production, whereas the C3a response in the presence of S5/1 was unaffected. Finally, desensitization experiments revealed a homologous desensitization of C3a after restimulation with C3a. In contrast, no cross-desensitization was observed upon stimulation with C5a. Furthermore, the C3a- and C5a-induced production of ROS of eosinophils was totally inhibited by pertussis toxin, indicating the involvement of guanine nucleotide-binding proteins (Gi-proteins). In summary, these results demonstrate that C3a is a potent activator for eosinophils initiating transient [Ca2+]i changes and production of reactive oxygen species. C3a therefore may play a part in the pathophysiology of diseases with eosinophil and complement activation.

Calcium↗
PubMed1994

The chemokine RANTES is more than a chemoattractant: characterization of its effect on human eosinophil oxidative metabolism and morphology in comparison with IL-5 and GM-CSF.

Eosinophils were shown to play a major role in the allergic inflammatory process leading to the clinical symptoms of atopic dermatitis. Only selected cytokines are capable of inducing a chemotactic response in eosinophils. In particular, the chemokine RANTES was recently shown to be a potent eosinophil chemotaxin. To examine the role of RANTES in eosinophil activation, we investigated the effect of RANTES and other chemokines on morphology and oxidative metabolism of highly purified eosinophils of normal nonatopic blood donors by assessment of functional as well as morphologic criteria. RANTES, and, to a lesser extent, MIP-1 alpha significantly induced the production of reactive oxygen species by human eosinophils, whereas MCP-1, MIP-1 beta, and interleukin (IL)-8/NAP-1 had no significant effects. RANTES stimulated only a subpopulation of the normal eosinophils. With the exception of IL-8, none of the cytokines tested had any significant effect on polymorphonuclear neutrophilic granulocytes. By scanning electron microscopy, RANTES induced characteristic changes that were completely abrogated in the presence of cytochalasin B. Based on functional and ultrastructural assays significant extracellular but not intracellular H2O2 production was detected and completely inhibited by cytochalasin B. Separation of eosinophils by discontinuous density gradients revealed the existence of two hypodense eosinophil populations, one which showed significantly reduced responses upon stimulation with RANTES. RANTES-induced production of reactive oxygen species was almost completely inhibited by staurosporine, wortmannin, or pertussis toxin. Based on these data it is evident that RANTES represents a potent eosinophil-specific activator of oxidative metabolism. Besides its chemotactic activity on T cells and eosinophils, therefore, RANTES may be involved in the functional activation of eosinophils in the skin of patients with atopic dermatitis.

Alkaloids↗
PubMed1994

TNF alpha-induced activation of eosinophil oxidative metabolism and morphology--comparison with IL-5.

Human dermal mast cells are capable of releasing cytokines, particularly preformed TNF alpha, upon appropriate stimulation. Mast cell activation in vivo was shown to be associated with an influx and activation of inflammatory cells, initially PMN (polymorphonuclear neutrophilic granulocytes) then eosinophils. In order to learn more about the mechanisms by which TNF alpha is capable of activating eosinophils, in the present study the effect of TNF alpha on morphology and function of highly purified normal eosinophils (> or = 95%) was examined. As estimated by transmission and scanning electron microscopy, TNF alpha-stimulated eosinophils appeared to be strictly adherent and flattened exhibiting a characteristic "hemispheric" shape. TNF alpha induced a dose-dependent, long-lasting production of reactive oxygen species as measured by lucigenin-dependent chemiluminescence (CL), even at a concentration of 0.001 U/ml. The maximal response upon stimulation with TNF alpha, however, was significantly lower than optimal effects induced by IL-5. TNF alpha-induced responses were completely inhibited by cytochalasin B and staurosporin, and partially blocked by pertussis toxin. Separation of eosinophils by discontinuous density gradients revealed the existence of at least two hypodense eosinophil populations with a distinct susceptibility to stimulation with TNF alpha. Based on functional assay systems, in contrast to a significant extracellular, only a small intracellular H2O2 production was detected. Accordingly, H2O2 production, detected by an ultrastructural technique, was observed only on the outer surface of the plasma membrane in the contact zones in between adjacent cells. Extracellular as well as intracellular production of H2O2 was completely inhibited by cytochalasin B. TNF alpha-induced activation of eosinophils is most probably mediated by binding to the 55 kD and the 75 kD TNF-receptor since both receptor molecules could be detected by FACS analysis and immune electron microscopy using receptor-specific antibodies. However, in contrast to its effect on eosinophil oxidative response, TNF alpha did not induce the release of significant concentrations of eosinophil cationic protein or eosinophil peroxidase in supernatants of cytokine-stimulated eosinophils, as detected by functional as well as immunological assay systems. These results clearly indicate that TNF alpha represents a potent eosinophil-activating cytokine which may be of relevance in the allergic inflammatory response.

Blood Proteins↗
PubMed1994

High prevalence of thyroid autoimmunity in idiopathic Addison's disease.

We have determined the incidence of autoimmune thyroid disorders in patients with Addison's disease. The material comprised 212 patients, 128 women and 84 men, aged 9-74 years. In 58 patients tuberculosis and in six patients other adrenal disorders were diagnosed. In the remaining 148 patients the auto-immune mechanism was the most probable cause of adrenocrotical insufficiency. In order to evaluate the thyroid abnormalities seen in patients with Addison's disease the T3, T4 (RIA), TSH (ELISA) and anti-thyroid autoantibodies were determined apart from routine clinical examination. Antimicrosomal, anti-thyroglobulin and anti-thyroperoxidase antibodies were measured in 91, 188 and 81 cases respectively. Thyrotoxicosis was diagnosed in 17 and primary hypothyroidism in 18 cases. Moreover, eight patients had evidence of subclinical hypothyroidism. The anti-thyroglobulin antibodies with titer ranging from 1:80 to 1:10,000 were detected in 66 patients, whereas antimicrosomal antibodies were found in 51 patients at a titer ranging from 1:80 to 1:9720. Autoantibodies against thyroid peroxidase were found in sera of 67 patients, with titer ranging from 1:2000 to 1:25,6000.

Addison Disease↗
PubMed1993

Granulocyte activation in bullous diseases: release of granular proteins in bullous pemphigoid and pemphigus vulgaris.

BACKGROUND: Eosinophil and polymorphonuclear granulocytes may be involved in the formation of blisters in bullous dermatoses, particularly bullous pemphigoid. OBJECTIVE: Our purpose was to evaluate the role of granulocyte activation in the pathogenesis of pemphigus vulgaris and bullous pemphigoid. METHODS: Levels of eosinophil cationic protein (ECP) and neutrophil-derived myeloperoxidase (MPO) in blister fluid and serum and levels of serum IgE were determined in patients with bullous pemphigoid (n = 12), those with pemphigus vulgaris (n = 9) and healthy volunteers (n = 12). RESULTS: In blister fluid and serum of patients with bullous pemphigoid, significantly elevated concentrations of ECP, MPO and IgE were detected as compared with controls. In contrast, ECP, MPO, and IgE levels in blister fluid and serum of patients with pemphigus vulgaris did not significantly differ from controls. Moreover, the MPO/ECP ratio in serum of patients with bullous pemphigoid was significantly decreased as compared with controls, whereas the MPO/ECP ratio in pemphigus vulgaris did not differ from controls, indicating a preferential activation of eosinophils in bullous pemphigoid only. In patients with bullous pemphigoid, serum levels of ECP and MPO significantly decreased during immunosuppressive therapy to levels similar to those of controls. CONCLUSION: Activated granulocytes, releasing their granular contents such as ECP and MPO, may be of importance for blister formation in bullous pemphigoid and may be useful for monitoring disease activity.

Aged↗
PubMed1993

Induction of intercellular adhesion molecule 1 (ICAM-1) expression in normal human eosinophils by inflammatory cytokines.

Intercellular adhesion molecule-1 (ICAM-1) functions as a ligand for lymphocyte function-associated antigen-1 (LFA-1), and thereby plays a crucial role in mediating cell-cell interactions in inflammatory reactions. Human eosinophils represent important effector cells in allergic skin diseases. To gain more insight into the capacity of eosinophils to physically interact with LFA-1-positive inflammatory leukocytes, in the present study ICAM-1 expression in eosinophils was investigated. Using fluorescence-activated cell sorter analysis, it could be shown that highly purified (> or = 95%) eosinophils from peripheral blood of non-atopic individuals do not constitutively express ICAM-1 molecules. However, stimulation of eosinophils with interferon gamma (IFN gamma), tumor-necrosis factor alpha (TNF alpha), or interleukin 3 (IL-3) markedly upregulated ICAM-1 surface expression in a time- and dose-dependent manner. Cytokine-induced ICAM-1 expression in human eosinophils was corroborated by Northern blot analysis. Accordingly, unstimulated eosinophils did not express significant amounts of ICAM-1 mRNA, but ICAM-1 mRNA expression could be markedly induced in these cells upon stimulation with IFN gamma plus TNF alpha. The combination of TNF alpha with either IFN gamma, IL-3, IL-5, or granulocyte/macrophage colony-stimulating factor (GM-CSF) increased ICAM-1 expression in a synergistic fashion, whereas IL-5 or GM-CSF by itself did not induce ICAM-1 expression. Cytokine-induced ICAM-1 expression was specific, because IL-1 alpha, IL-1 beta, IL-2, IL-4, IL-6, IL-7, IL-8, C5a, and platelet-activating factor did not significantly affect eosinophil ICAM-1 surface expression. In summary, these studies indicate that eosinophils may be activated to express the adhesion molecule ICAM-1 upon stimulation with selected inflammatory cytokines, which may allow adhesion-mediated cross-talk between eosinophils and LFA-1-positive cells. In addition, these data demonstrate for the first time a role for IL-3, IL-5, and GM-CSF in regulation of ICAM-1 expression in human cells.

Antigens, CD↗
PubMed1993

Human cell adhesion molecule uvomorulin is differentially expressed in various skin tumors.

The cell adhesion molecule uvomorulin is important in cell recognition processes, both during tissue formation in embryonic development and in the maintenance of adult epithelia. In addition, uvomorulin appears to play a crucial role in carcinogenesis. Therefore, in the present study, the expression of uvomorulin in normal human skin and several benign and malignant proliferative skin lesions was evaluated by immunofluorescence microscopy using affinity purified antibodies. In normal human epidermis, basal and suprabasal keratinocytes showed a strong and homogeneous staining of the cell membrane. In contrast, uvomorulin expression was decreased in squamous cell, as well as in solid basal cell, carcinoma. Interestingly, solid basal cell carcinoma showed a dimorphic staining pattern with a reduced fluorescence of the inner cell layers and normal staining of the peripheral basal cells. In contrast, no such dimorphic staining pattern could be observed in squamous cell carcinoma, in which uvomorulin expression was homogeneously reduced. Decreased expression of uvomorulin was not specific for malignant skin lesions, since it could also be observed in condylomata acuminata. These studies demonstrate that human uvomorulin is differentially expressed in proliferative skin disorders, which may account at least in part for the differences observed in the clinical course between squamous cell and basal cell carcinoma.

Cadherins↗
PubMed1992

High-dose UVA1 therapy in the treatment of patients with atopic dermatitis.

BACKGROUND: Besides glucocorticosteroids, there is currently no known effective therapy for patients with acute atopic dermatitis. OBJECTIVE: The therapeutic effectiveness of high-dose UVA1 irradiation in the management of patients with acute exacerbation of atopic dermatitis was examined. METHODS: Patients in the high-dose UVA1 group (n = 15) were irradiated with 130 joules/cm2 UVA1; the control group (n = 10) was treated with UVA-UVB therapy in a minimal erythema dose-dependent manner (total number of treatments 15). RESULTS: High-dose UVA1 irradiation was found to induce a significant clinical improvement of atopic dermatitis (p less than 0.001). In comparison with UVA-UVB therapy, significant differences in favor of high-dose UVA1 were observed (p less than 0.01). High-dose UVA1, but not UVA-UVB treatment, significantly reduced the elevated serum level of eosinophil cationic protein in patients with atopic dermatitis (p less than 0.003). CONCLUSION: These studies indicate that high-dose UVA1 irradiation may represent a novel phototherapeutic modality for the treatment of patients with an acute exacerbation of atopic dermatitis.

Adult↗
PubMed1992

Ultraviolet radiation effects on human keratinocyte ICAM-1 expression: UV-induced inhibition of cytokine-induced ICAM-1 mRNA expression is transient, differentially restored for IFN gamma versus TNF alpha, and followed by ICAM-1 induction via a TNF alpha-like pathway.

Human keratinocytes (KC) during the course of inflammatory dermatoses strongly express the surface molecule ICAM-1, which plays an important role in the generation of the epidermal inflammatory infiltrate by mediating leukocyte-keratinocyte interactions. Accordingly, KC ICAM-1 expression is known to be induced in vivo and in vitro by cytokines either via the TNF alpha/TNF beta or via the IFN gamma-mediated pathway. In contrast, ultraviolet (UV) radiation previously has been found to potently inhibit cytokine-induced KC ICAM-1 surface expression by a sublethal mechanism. In order to further define this novel immunosuppressive effect of UV light, the effects of in vitro UV radiation on ICAM-1 mRNA expression in transformed human KC (KB cells) were examined. Accordingly, UV light (0-100 J/m2) inhibited IFN gamma- as well as TNF alpha-induced ICAM-1 mRNA expression, if KC were cytokine stimulated immediately after irradiation. After a 12-h incubation period, however, IFN gamma responsiveness was found to be restored in irradiated cells, whereas restoration of responsiveness to TNF alpha required at least a 24-h recovery phase. Moreover, UV light alone did not alter ICAM-1 mRNA levels after 4, 12, or 24 h. After 48 h, however, a significant increase in ICAM-1 mRNA and surface expression in UV-irradiated KC could be observed. In addition, this increase could be superinduced by stimulation of irradiated KC with IFN gamma, but not with TNF alpha. UV-induced upregulation of ICAM-1 expression could be mimicked by stimulating unirradiated cells with supernatants derived from UV-irradiated cells. Addition of biologically active anti-TNF alpha antibodies to UV-irradiated cells or to supernatants derived from UV-irradiated KC, however, did not even partially abolish this ICAM-1-inducing activity. UV light thus seems to affect KC ICAM-1 mRNA expression in a biphasic manner: an early period of inhibition of cytokine-induced ICAM-1 expression is transient and followed by restoration of responsiveness to ICAM-1-inducing cytokines. Moreover, UV itself is able to induce ICAM-1 mRNA expression at this later time point via a TNF alpha-like pathway. These studies identify UV irradiation as a potent modulator of cytokine regulated ICAM-1 gene transcription with the capacity to induce both inhibitory as well as enhancing effects.

Blotting, Northern↗
PubMed1992

Serum eosinophil cationic protein (ECP) is a sensitive measure for disease activity in atopic dermatitis.

Atopic dermatitis (AD) is characterized by alterations in cellular and humoral immunity including elevated serum levels of IgE, IL-2 receptor (IL-2R) and eosinophil cationic protein (ECP). In order to evaluate the relevance of these serum parameters as indicators of disease activity, the concentrations of IgE, IL-2R and ECP were measured in serum samples of patients with an acute exacerbation of AD (n = 19) on admission to hospital and every 6 days up to discharge, and compared with those from normal non-atopic controls (n = 15). The severity of the disease in the AD patients was examined using an established clinical scoring system. On admission, AD patients showed significantly elevated serum levels of IgE, IL-2R and ECP compared with normal controls (P less than or equal to 0.0001). Clinical improvement was associated with a decrease of both the clinical score (P less than or equal to 0.001) and serum ECP levels (P less than or equal to 0.005). No significant changes in serum IgE and serum IL-2R were observed. In addition, there was a significant correlation between serum ECP and the clinical score (R = 0.67, P less than or equal to 0.001). These data indicate that serum ECP may be a helpful tool for monitoring disease activity in AD.

Acute Disease↗