Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients with severe arthralgia associated with palmoplantar pustulosis (PPP) were treated with oral cyclosporine A (CsA). Clinical efficacy was assessed on a 0-4 point scale for erythema, desquamation, infiltration, and pustulation, and on a 0-3 point pain scale. Skin lesions and arthralgia improved within twelve weeks with low dose CsA ranging from 2.1 to 2.2 mg/kg/day. High levels of plasma interleukin-6 (IL-6) were reduced to the normal range.
J Dermatol 1995 Jul
PMID:Successful treatment of severe arthralgia associated with palmoplantar pustulosis with low-dose oral cyclosporine A. 756 Apr 44

To evaluate the contribution of peripheral blood monocytes (PBMC) to epidermotropic inflammatory reactions in psoriasis, using an enzyme-linked immunosorbent assay we measured spontaneous interleukin-8 (IL-8) production in PBMC obtained from patients with psoriasis. IL-8 production in the psoriatic PBMC was significantly higher than that in normal control PBMC. Plasma IL-8 levels in psoriatic patients were also moderately increased compared to normal control levels. IL-8 production in PBMC was closely related to the clinical severity of psoriasis and to the response to treatment, including systemic methotrexate (MTX) treatment and tonsillectomy. IL-8 production in PBMC was also positively related to the production of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in these cells. We speculate that the chemotactic cytokine IL-8 contributes to the development of psoriatic skin lesions, and mediates inflammatory reactions from the inflammatory focus to the psoriatic lesions.
J Dermatol Sci 1995 Jul
PMID:Increased spontaneous production of IL-8 in peripheral blood monocytes from the psoriatic patient: relation to focal infection and response to treatments. 757 39

Psoriasis represents an inflammatory skin disorder which is characterized by a marked hyperproliferation of keratinocytes in association with vascular expansion, fibroblast activation, leukocyte infiltration, alterations of eicosanoid metabolism and of cytokine production. However, it is unclear at present whether these changes may be a cause or a result of the significantly increased keratinocyte turnover. More than one mechanism is involved in triggering active psoriasis, particularly a genetic predisposition and environmental factors affecting the immune system. Most of the therapeutic regimes used for the treatment of psoriasis are immunosuppressive. Therefore, it is tempting to speculate that a specific defect of the immune system represents an important pathogenic principle in psoriasis. There are several lines of evidence that changes in cytokine production by keratinocytes and immunocompetent cells in the skin of the patients (particularly of interleukin-6 and TGF-alpha) may play an important role in the propagation of the inflammatory response in psoriasis. Further studies are required to reveal the role of a local T-cell activation as a basic mechanism for initiation and maintenance of the psoriatic inflammatory response. Accordingly, parameters, such as the evaluation of cytokine production in vitro and in vivo, as well as the measurement of cellular activation products, may be useful tools for diagnosis and monitoring of psoriasis.
J Dermatol Sci 1993 Jun
PMID:The role of cytokines in the psoriatic inflammation. 769 46

It has been proposed that interleukin-6 may play a role in the pathogenesis of autoimmune diseases like lupus erythematosus. We have therefore investigated the immunoreactivity of IL-6 in 32 skin biopsies of 23 patients suffering from chronic discoid lupus erythematosus (n = 16), subacute cutaneous lupus erythematosus (n = 5) and systemic lupus erythematosus (n = 5) as well as in uninvolved skin (n = 6) and in normal skin from healthy volunteers (n = 3). Increased immunohistochemical staining was detectable in 14 of 26 biopsies from lesional skin. The remaining biopsies from lesional, non-lesional and normal skin displayed only minimal or no reactivity, but 8 out of 12 lupus erythematosus patients had been pretreated with local or systemic antiinflammatory drugs. Irrespective of the LE subtype, immunolabelling was generally most intense in the basal layer of the epidermis, with additional intense suprabasal staining in sections from 2 of 5 SLE patients. Preferential production of IL-6 in the lower parts of the epidermis was confirmed by RNA in situ hybridization. No correlation was found between the deposition of immunoglobulins and complement at the dermo-epidermal junction and IL-6 expression in keratinocytes. These data suggest that IL-6 may be involved in LE although its exact role in the pathogenesis of the disease needs to be further elucidated.
Exp Dermatol 1995 Feb
PMID:Interleukin-6 expression in the skin of patients with lupus erythematosus. 775 33

Recent investigations have revealed the involvement of cytokines in the pathogenesis of psoriasis. This study examined the amount of inflammatory cytokines--interleukin-1 (IL-1), interleukin-6 (IL-6) and granulocyte macrophage colony-stimulating factor (GM-CSF)--released into the supernatants of organ cultures of involved and uninvolved skin from psoriatic patients and normal skin from healthy individuals. Bioassays were employed to detect the activities of IL-1 and IL-6. Enzyme-linked immunosorbent assay (ELISA) methods were used to quantitate immunoreactive IL-1 alpha, IL-1 beta, IL-6 and GM-CSF. The activity of IL-1 in uninvolved psoriatic skin was found to be increased relative to that in involved and normal skin, while immunoreactive IL-1 beta was found only in involved skin. A neutralization experiment showed that bioactive IL-1 was mostly attributable to IL-1 alpha. Uninvolved psoriatic skin also secreted higher amounts of both bioactive and immunoreactive IL-6 compared with involved skin. Immunoreactive GM-CSF was detected in uninvolved skin only. These cytokines detected in uninvolved skin may have been released from epidermal or mesenchymal cells, since uninvolved skin contained fewer inflammatory infiltrates. Our results offer additional evidence that increased amounts of inflammatory cytokines in uninvolved skin may provide a preliminary condition and play important roles in the initial events in the evolution of psoriatic lesions.
Arch Dermatol Res 1995
PMID:Detection of inflammatory cytokines in psoriatic skin. 776 87

Localized scleroderma has been reported to be accompanied by immunological abnormalities related to B cells, but little is known about T-cell activation in this disease. In this study, serum levels of interleukin-2 (IL-2), interleukin-4 (IL-4) and interleukin-6 (IL-6), which are known to be released by activated T cells, were determined using a sensitive enzyme-linked immunosorbent assay in 48 patients with localized scleroderma and 20 with systemic sclerosis, and in 20 healthy control subjects. IL-2, IL-4 and IL-6 were detected in serum from patients with localized scleroderma but not in that from healthy controls. The presence of antihistone antibodies correlated significantly with elevated IL-4 and IL-6 levels. Decreased serum levels of IL-2, IL-4 and IL-6 paralleled improvement in cutaneous sclerosis. Frequent detection of these lymphokines in serum from patients with localized scleroderma reflects T-cell activation in this disorder.
Arch Dermatol Res 1995
PMID:Demonstration of interleukin-2, interleukin-4 and interleukin-6 in sera from patients with localized scleroderma. 776 91

Tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and granulocyte monocyte-colony stimulating factor (GM-CSF) were measured in serum and involved and uninvolved skin blister fluids of 20 psoriatic patients and 10 healthy subjects, by enzyme immunoassay. TNF-alpha and IL-6 were always detectable in involved skin blister fluids, while GM-CSF was detected only in 45% of these samples. TNF-alpha, IL-6 and GM-CSF were detected in 95, 100 and 10% of uninvolved skin blister fluid samples, respectively. TNF-alpha and IL-6 were found in 50 and 30% of control blister fluids, while GM-CSF was never detected. In serum, TNF-alpha was detected in 75% of patients and in 70% of controls; IL-6 in 45% of patients and in no controls; and GM-CSF in 35% of patients and in 20% of the controls. The median TNF-alpha and IL-6 levels in involved skin were statistically higher than those of both uninvolved and control skin blister fluids. TNF-alpha and IL-6 levels in blister fluids obtained from both involved and uninvolved skin were higher than those of the patients' sera. GM-CSF, when present in involved skin blister fluids, showed correlated levels with the other cytokines (TNF-alpha: R = 0.85, P = 0.004; IL-6: R = 0.72, P = 0.03). TNF-alpha was highly correlated with IL-6 (R = 0.78, P < 0.00001) in involved skin blister fluids. TNF-alpha and IL-6 levels of involved skin blister fluids showed significant correlations with the psoriasis area and severity index scores in the patients, suggesting a direct relationship between these cytokines and the clinical manifestations of the disease. Moreover, the TNF-alpha levels were particularly related to the erythema scores in the patients, further supporting evidence of their role in the pathogenesis of the disease.
Clin Exp Dermatol 1994 Sep
PMID:Correlated increases of tumour necrosis factor-alpha, interleukin-6 and granulocyte monocyte-colony stimulating factor levels in suction blister fluids and sera of psoriatic patients--relationships with disease severity. 795 93

Interleukin-6 (IL-6) is a multipotential cytokine which may act as a growth factor for keratinocytes. The epidermal hyperplasia of psoriasis may be explained in part by an overproduction of this cytokine. We have previously shown by in situ hybridization that IL-6 mRNA is most strongly expressed in the peripheral lesion of an advancing psoriatic plaque. In the present study, we investigated whether there were differences between the expression of IL-6 in untreated psoriatic epidermis and the lesion during the course of clinical improvement. In the untreated psoriatic lesion, the weak expression of IL-6 mRNA was localized in the lower epidermis. However, IL-6 mRNA was not detected in the clearly improved lesion. In the improving lesion, with clinically less scaling, less induration, and histologically thinner epidermis, IL-6 mRNA-expressing keratinocytes were detectable in a greater proportion of the total epidermal components than in the untreated, fully developed lesion. These results showed that IL-6 mRNA was strongly expressed in lesions with moderate epidermal hyperproliferation, indicating that this cytokine may play a role in the transitional phase during the course of improvement as well as in the lesion's formation.
J Dermatol 1994 May
PMID:In situ expression of interleukin-6 in psoriatic epidermis during treatment. 805 14

Normal human melanocytes and melanoma cells have been reported to produce several cytokines. Previously we demonstrated that neonatal human melanocyte proliferation and tyrosinase activity are inhibited by interleukin-1 alpha, tumor necrosis factor-alpha, and interleukin-6. We have now also shown that interleukin-1 beta induces an inhibiting effect on neonatal melanocyte tyrosinase activity with little effect on melanocyte proliferation. We investigated the ability of neonatal and adult human melanocytes to synthesize interleukin-1 alpha and beta. By immunocytochemistry, using monoclonal antibodies against interleukin-1 alpha and beta, we observed that neonatal and adult melanocytes stain positively for both cytokines. Flow-cytometric analysis revealed that the percentage of melanocytes positive for interleukin-1 alpha was always greater than that for interleukin-1 beta. The ability of neonatal and adult melanocytes to synthesize interleukin-1 alpha and beta was further confirmed using the polymerase chain reaction. These results clearly indicate that human melanocytes synthesize interleukin-1 alpha and beta, and that these cytokines may function as autocrine and/or paracrine regulators of cells in the epidermis.
J Invest Dermatol 1994 May
PMID:Synthesis of interleukin-1 alpha and beta by normal human melanocytes. 817 58

The present study was undertaken to investigate whether modulation of interleukin-6 and interleukin-1 production occurs owing to keratinocyte-fibroblast interaction. Normal human keratinocytes or squamous carcinoma cells were cultured either alone or in the presence of human foreskin fibroblasts or murine 3T3 cells. All cells tested produced interleukin-6, and interleukin-6 levels were markedly increased when normal or malignant keratinocytes were co-cultured with fibroblasts. The bioassay (species independent) and enzyme-linked immunosorbent assay (specific for human interleukin-6) together with use of complementary DNA probes specific for human or murine interleukin-6 revealed that fibroblasts are responsible for increased interleukin-6 levels. Moreover, interleukin-6 levels were increased when fibroblasts were cultured in conditioned media derived from normal human keratinocytes and squamous carcinoma cells-4 cultures. Interleukin-1 alpha secreted by normal human keratinocytes and squamous carcinoma cells-4 cells was mainly responsible for the increased interleukin-6 production in fibroblasts. Although interleukin-1 activity increased linearly with the incubation time in squamous carcinoma cells-4 monocultures, interleukin-1 activity was low and remained unchanged in squamous carcinoma cells-4/3T3 co-cultures. Low interleukin-1 activity was most probably not due to inhibition of interleukin-1 alpha production in squamous carcinoma cells-4/3T3 co-cultures because interleukin-1 alpha messenger RNA expression in squamous carcinoma cells-4 cells remained unchanged in the presence of 3T3 cells. Furthermore, when 3T3 cells were incubated in conditioned medium derived from squamous carcinoma cells-4 cells, high interleukin-1 activity decreased to an undetectable level, suggesting that fibroblasts are involved in the suppression of interleukin-1 activity. The remaining interleukin-1 activity, however, was sufficient for maximal induction of interleukin-6 production in fibroblasts. These results suggest that the interaction between epithelial and mesenchymal cells is at least partly initiated by interleukin-1 alpha secreted by the activated epithelial cell during skin injury or tumor invasion. Interleukin-1 in turn can induce modulation of the synthesis of various pro-inflammatory mediators and proteases in surrounding fibroblasts. An enhanced proteolytic activity and/or a possible induced production of an interleukin-1 inhibitor in fibroblasts and/or a receptor-mediated interleukin-1 consumption by fibroblasts will cause a decrease in interleukin-1 activity and thus exert a negative feedback.
J Invest Dermatol 1993 Sep
PMID:Modulation of IL-6 production and IL-1 activity by keratinocyte-fibroblast interaction. 837 Sep 68


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