Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphocytes from twenty-five patients with atopic dermatitis were investigated for their in vitro reactivity to stimulation with tuberculin (PPD), lipopolysaccharide (LPS), phytohaemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM). The response to a low dose of Con A was increased, and the reactivity in unstimulated cultures tended to be lower than similar cultures from the control group. Addition of inactivated autologous plasma to the cultures had an inhibitory effect, when the plasma came from patients with high levels of IgE. The patients' in vitro reactivity to PPD in a leucocyte migration test was equal to that found in normal persons and no effect was observed after addition of autologous serum. The mean percentage of E rosette forming cells was significantly reduced in patients with high levels of IgE. The number of EAC rosette forming cells was within normal range. It is hypothesized that the observations could reflect the existence of suppressor mechanisms in patients where the immune system is strongly stimulated.
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PMID:PPD and mitogen responsiveness of lymphocytes from patients with atopic dermatitis. 84 45

Endothelial leucocyte adhesion molecule-1 (ELAM-1) is a recently described endothelial surface glycoprotein which is inducible by interleukin 1 (IL-1), tumour necrosis factor-alpha (TNF-alpha) or bacterial lipopolysaccharide (LPS). Using an immunohistochemical technique and a monoclonal antibody (1.2B6) specific for ELAM-1 we have found marked vascular endothelial expression of ELAM-1 in many cutaneous inflammatory disorders, including allergic contact dermatitis, atopic dermatitis and psoriasis, and in dermal infiltrates associated with benign, premalignant and malignant keratinocyte proliferation. In normal skin, minimal levels of ELAM-1 expression were detected. In psoriasis, double-immunoenzyme staining studies revealed a close spatial relationship between ELAM-1 expression and neutrophil margination, suggesting a functional link. Recombinant human interferon-gamma (30 micrograms) injected intradermally in normal adult human volunteers did not substantially upregulate ELAM-1 in contrast to its marked effect on intercellular adhesion molecule-1 (ICAM-1) expression, indicating that this cytokine is probably not involved in ELAM-1 induction in vivo. These results indicate that ELAM-1 is widely induced in cutaneous inflammation with a time course of expression that is longer than that observed in vitro. As ELAM-1 acts as an adhesion ligand for neutrophils, and perhaps monocytes, the expression of this molecule in cutaneous lesions is likely to be an indication of the ability of vascular endothelium to recruit these cells from the circulation. Furthermore, the cytokine inducibility of ELAM-1 is indirect evidence for functional interactions between perivascular mononuclear cells, other resident cells and the blood vessel wall.
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PMID:Endothelial leucocyte adhesion molecule-1 (ELAM-1) expression in cutaneous inflammation. 170 95

In 31 adult patients with atopic dermatitis, the capacity to secrete interleukin-1 (IL-1) from peripheral blood mononuclear cells and from purified monocytes was investigated following stimulation with lipopolysaccharide. We also measured soluble interleukin-2 receptor levels (sIL-2R) and CD-8 receptor in serum from some of the patients in order to estimate the degree of lymphocyte stimulation in vivo. We observed that purified monocytes from patients with atopic dermatitis released more IL-1 than unseparated blood mononuclear cells did and also had significantly greater IL-1 activity than non-atopic donors. Addition of histamine in concentrations of 10(-7) to 10(-4) M did not suppress, but rather augmented the IL-1 activity release. An increased monocyte-IL-1 release could lead to increased T lymphocyte activity. We observed that 60% of the patients had increased sIL-2R concentrations in serum. There was no correlation between serum IgE and sIL-2R. Our observations indicate that monocytes in atopic dermatitis patients release increased quantities of IL-1, supporting an augmented T lymphocyte activation in the patients.
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PMID:Interleukin-1 release from peripheral blood monocytes and soluble interleukin-2 and CD8 receptors in serum from patients with atopic dermatitis. 198 Sep 72

The immunomodulating cytokines, tumour necrosis factor/cachectin (TNF) and lymphotoxin (LT) are thought to play an essential role as mediators of inflammatory reactions. To evaluate the role of TNF and LT in atopic dermatitis (AD) and psoriasis, we investigated their production by mononuclear cells (MNC) in vitro. The 24-h supernatants of lipopolysaccharide (LPS)- and phytohaemagglutinin (PHA)-stimulated and unstimulated MNC from 26 patients with AD and 20 with psoriasis and from 17 non-atopic healthy controls were tested for the concentrations of TNF and LT using an ELISA technique. In patients with AD, TNF levels were significantly decreased in the supernatant of PHA-stimulated (P less than or equal to 0.005) and LPS-stimulated (P less than or equal to 0.02) MNC in comparison to controls. There was no significant difference in TNF production between psoriatic patients and the control group. Release of LT in the supernatant of PHA-stimulated MNC by patients and controls did not differ significantly. There was no significant spontaneous production of TNF and LT by MNC of patients and controls. These studies indicate that different immunomodulating mechanisms are responsible for triggering the inflammatory response in AD and psoriasis.
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PMID:Immunomodulating cytokines in atopic dermatitis and psoriasis: production of tumour necrosis factor and lymphotoxin by mononuclear cells in vitro. 235 11

A monoclonal antibody is described that was generated by immunizing mice with cultured human blood monocytes. The antibody (27E10) belongs to the IgG1 subclass and detects a surface antigen at Mr 17,000 that is found on 20% of peripheral blood monocytes. The antigen is increasingly expressed upon culture of monocytes, reaching a maximum between days 2 and 3. Stimulation of monocytes with interferon-gamma (IFN-gamma), 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and lipopolysaccharide (LPS) but not with N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) increased the 27E10 antigen density. The amount of 27E10-positive cells is not or is only weakly affected. The antigen is absent from platelets, lymphocytes, and all tested human cell lines, yet it cross-reacts with 15% of freshly isolated granulocytes. By using the indirect immunoperoxidase technique, the antibody is found to be negative on cryostat sections of normal human tissue (skin, lung, and colon) and positive on only a few monocyte-like cells in liver and on part of the cells of the splenic red pulp. In inflammatory tissue, however, the antibody is positive on monocytes/macrophages and sometimes on endothelial cells and epidermal cells, depending on the stage and type of inflammation, e.g., BCG granulomas are negative, whereas psoriasis vulgaris, atopic dermatitis, erythrodermia, pressure urticaria, and periodontitis contain positively staining cells. In contact eczemas at different times after elicitation (6 hr, 24 hr, and 72 hr), the 27E10 antigen is seen first after 24 hr on a few infiltrating monocytes/macrophages, which increase in numbers after 72 hr. From this it is concluded that the antibody 27E10 detects an antigen expressed by a subset of peripheral blood monocytes. In situ the antigen is found only in inflammatory tissues and is absent from normal resident mononuclear phagocytes.
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PMID:A monoclonal antibody to a subset of human monocytes found only in the peripheral blood and inflammatory tissues. 372 15

It has been suggested that in atopic eczema (AE) a reduced lymphocyte response to T-cell mitogens in vitro is secondary to altered production of cytokines or inflammatory mediators. We investigated, in parallel, the mitogen-induced T-cell proliferation, monocyte interleukin-1 beta (IL-1 beta) production, and prostaglandin E2 (PGE2) production of monocytes and of peripheral blood mononuclear cells (PBMC) in AE patients and non-atopic controls. After stimulation with concanavalin A (Con A) PBMC of AE patients showed a significantly reduced proliferative response compared with the controls. The monocyte production of IL-1 beta after stimulation with lipopolysaccharide (LPS) was significantly decreased in AE. No differences between AE patients and controls were observed with regard to the PGE2 production of PBMC after stimulation with Con A or the monocyte release of PGE2 after LPS stimulation. Because IL-1 plays a central role in the activation of T-cell proliferation, the decreased monocyte IL-1 beta production may provide a plausible explanation for the reduced mitogen response of T cells in AE.
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PMID:Decreased monocyte interleukin-1 beta production in atopic eczema. 771 54

Fibrin deposition is an important histopathological feature of inflammatory skin lesions and is mediated in part, by procoagulants generated by mononuclear leucocytes (MNL). We examined whether MNL from patients with atopic dermatitis or psoriasis generate enhanced procoagulant activity (PCA). MNL isolated from the peripheral blood of 15 healthy control individuals, 15 patients with atopic dermatitis and 15 patients with psoriasis were incubated for 24 h in the presence or absence of bacterial lipopolysaccharide (LPS). MNL or the cell culture supernatants were then added to recalcified human plasma to determine the clotting time. We found that in both atopic dermatitis and psoriasis MNL cultured in the presence or absence of LPS expressed greatly enhanced PCA (p < 0.01 to < 0.002). Supernatants from MNL cultures from patients with psoriasis, but not those from patients with atopic dermatitis, also generated augmented PCA (p < 0.002). In psoriasis, PCA normalized after successful topical treatment with anthralin. We conclude that enhanced PCA is a characteristic feature of MNL in both atopic dermatitis and psoriasis. In psoriasis the enhanced PCA is directly related to disease activity.
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PMID:Enhanced procoagulant activity of mononuclear leukocytes in patients with atopic dermatitis and psoriasis. 837 92

In this study we evaluated antigen-specific in vitro responses of peripheral blood lymphocytes to lipopolysaccharide (LPS)-depleted food allergens in children who reacted to food challenge (cow's milk or hen's egg) with a deterioration of their atopic dermatitis (AD). Some of the children showed immediate symptoms (urticaria, bronchial asthma or gastrointestinal symptoms) as well. The proliferation of casein-stimulated lymphocytes from children reacting to cow's milk (age 0.7-5.9 years) was significantly higher (P < 0.01) than the proliferation of lymphocytes from 15 children with AD without milk allergy (age: 2.1-9.1 years). Twenty-eight T-cell clones (TCC) were established from the blood of three children sensitized to cow's milk and hen's egg who reacted to double-blind, placebo-controlled oral food challenge both with a deterioration of AD and with immediate symptoms. Surprisingly, 16 of 28 casein- or ovalbumin-specific TCC were CD8+. All TCC produced high amounts of IFN-gamma upon stimulation with concanavalin A. In addition, 75% of the CD4+ TCC and 44% of the CD8+ TCC secreted IL-4. Our results indicate that: (i) food-specific proliferation of blood lymphocytes can be detected in patients with clinically relevant food allergy with LPS-depleted allergens in vitro and (ii) circulating food-specific lymphocytes are CD4+ and CD8+ T cells with the capacity of producing both type 1 and type 2 cytokines.
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PMID:The role of circulating food antigen-specific lymphocytes in food allergic children with atopic dermatitis. 897 15

Macrophage-derived chemokine (MDC)/CCL22 is a CC chemokine active on dendritic cells (DC), NK cells and Th2 lymphocytes. The present study was aimed at comprehensively investigating MDC production in vitro and in vivo. DC were the most potent producers of MDC among leukocytes tested. Endothelial cells did not produce MDC under a variety of conditions. Signals that induce maturation (lipopolysaccharide, IL-1, TNF, CD40 ligand, recognition of bacteria and yeast) dramatically augmented MDC production, and dexamethasone and vitamin D3 blocked it. Prostaglandin E(2), which blocked the acquisition of IL-12 production and the capacity to promote Th1 generation, did not affect MDC production. Using mass spectrometry-based techniques, DC supernatants were found to contain N-terminally truncated forms of MDC [MDC(3-69), MDC(5-69) and MD(C7-69)] as well as the full-length molecule. In vivo, CD1a(+), CD83(+), MDC(+) DC were found in reactive lymph nodes, and in Langerhans' cell histiocytosis. Skin lesions of atopic dermatitis patients showed that CD1a(+) or CD1b(+) DC, and DC with a CD83(+) phenotype were responsible for MDC production in this Th2-oriented disorder. Thus, DC are the predominant source of MDC in vitro and in vivo under a variety of experimental and clinical conditions. Processing of MDC to MDC(3-69) and shorter forms which do not recognize CCR4 is likely to represent a feedback mechanism of negative regulation.
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PMID:Dendritic cells as a major source of macrophage-derived chemokine/CCL22 in vitro and in vivo. 1124 Dec 86

This study was performed to determine whether or not IL-18, formerly called IFN-gamma-inducing factor, is involved in the pathogeneses of allergic disorders. Peripheral blood mononuclear cells (PBMC) were obtained from patients with allergic bronchial asthma (BA), patients with atopic dermatitis (AD) and controls who did not have any allergic disease, and then cultured with lipopolysaccharide (LPS) or phytohaemagglutinin (PHA). The concentrations of IL-18, IFN-gamma and IL-13 in supernatant fluids were determined by enzymatic immunoassaying, and the expression of IFN-gamma messenger (m) RNA in the cells was measured by colorimetric microplate assaying. IL-18 secretion in the BA patients (geometric mean (gm) = 189 pg/ml) and AD patients (gm = 172 pg/ml) was significantly higher than that in non-allergic controls (gm = 118 pg/ml). In contrast, IFN-gamma secretion in the BA patients (gm = 7.3 IU/ml) and AD patients (gm = 6.8 IU/ml) was significantly lower than that in non-allergic controls (gm = 20.7 IU/ml). The amounts of IL-13 in supernatant fluids and IFN-gamma mRNA in cells were not statistically different among the BA patients, AD patients and non-allergic controls. The possible involvement of IL-18 in allergic disorders is discussed.
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PMID:Increased secretion of IL-18 in vitro by peripheral blood mononuclear cells of patients with bronchial asthma and atopic dermatitis. 1170 60


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