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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors evaluate the involvement of various cytokines (interleukin-1, interleukin-2, interleukin-4, interleukin-6, tumor necrosis factor alpha and gamma-interferon) in the pathogenesis of multiple sclerosis. The cytokines might participate in nervous tissue damage by promoting demyelination and oligodendrocyte injury or by enhancing local immune response. In addition, several authors reported increased levels of some cytokines in serum and cerebrospinal fluid of patients with multiple sclerosis. These findings suggest that cytokines can play a significant role in the immunopathogenesis of the disease.
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PMID:Cytokines in the pathogenesis of multiple sclerosis. 129 76

Two sublines of L929 cells with different interferon (IFN)-producing capacities synthesized IFN and interleukin-6 (IL-6) simultaneously in response to Sendai virus infection. IFN pretreatment primed the production of both cytokines. However, the difference in IL-6 production between the "high and low producer" L-cell sublines was about one magnitude of order larger than in the case of their IFN production. The determination of the corresponding mRNA levels also reflected this difference.
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PMID:Interferon pretreatment regulates interferon and interleukin-6 production in L929 cells in a coordinated manner. 131 62

Interleukin-6 (IL-6) has actions on a variety of endocrine tissues. The cytokine is secreted by cells of the anterior pituitary and endocrine pancreas and has recently been shown to be produced by cultures of thyroid epithelial cells. In this study we have examined some of the factors which regulate IL-6 release from an immortalized human thyroid line (HTori3). IL-6 release over 24 h was stimulated by TSH (5000 microU/ml), by forskolin (0.01 mmol/l), by fetal calf serum (1-20%) and by epidermal growth factor (20 ng/ml). Stimulation was also apparent with gamma-interferon and with tumour necrosis factor at concentrations known to enhance class II major histocompatibility antigen expression by thyroid epithelium. The most potent factor tested was interleukin-1 (IL-1), which controls IL-6 release from other cell types. Threefold stimulation was found with 1 U/ml rising to 350-fold with 1000 U/ml. The effect of IL-1 took 2 h to develop and was blocked by cycloheximide (100 mumol/l). Stimulation was not markedly inhibited by pertussis toxin. Many of the actions of IL-1 are mediated by prostaglandin E2 (PGE2). At concentrations as low as 30 nmol/l, PGE2 stimulated IL-6 release but the maximum stimulation obtained with PGE2 was only threefold. The effect of IL-1 was not inhibited by indomethacin. These data provide further evidence that IL-6 is produced by human thyrocytes. The effect of IL-1 has not been demonstrated previously. Stimulation of IL-6 release by IL-1 did not appear to be mediated by prostaglandin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Release of interleukin-6 by human thyroid epithelial cells immortalized by simian virus 40 DNA transfection. 131 54

Interleukin-6 (IL-6) has various biological activities including growth stimulation and maturation of B cells into antibody-producing cells, growth stimulation of murine hybridoma and plasmacytoma cells, induction of acute phase proteins, activation of T cell functions, triggering differentiation of various hematopoietic cells, and inhibition of growth of the human ductal breast carcinoma cell line T-47. Recently it was found that IL-6 also has the ability to enhance natural killer (NK) cell activity. In the present study the possible role of IL-6 as a regulator of NK cell-mediated cytotoxicity (NK-CMC) was evaluated. It was found that IL-6 reduced the sensitivity of T-47 cells (a ductal breast carcinoma cell line) to NK-CMC. The mechanism of IL-6-induced protection was studied. IL-6 had no effect on the level of conjugate formation between T-47 cells and NK cells. However, IL-6 reduced the number of dead conjugated T-47 cells. IL-6-treated T-47 cells were also found to be as sensitive as the nontreated cells to the lytic effect of NK cytotoxic factor (NKCF). However, IL-6 appeared to reduce the ability of T-47 cells to induce release of NKCF from NK cells following conjugate formation. Therefore, it is suggested that IL-6 protects T-47 cells from natural killing by the same mechanism as interferon.
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PMID:Interleukin-6 protects ductal breast carcinoma cells from MHC-unrestricted cell-mediated cytotoxicity. 132 93

We obtained peripheral blood mononuclear cells from 12 chronic hepatitis Type B patients, 12 Type C patients, and 15 healthy volunteers, and investigated the effects of OK-432, a streptococcal preparation, on in vitro production of 3 types of cytokines. Mononuclear cells in a concentration of 1 x 10(6) cell/ml were prepared in the culture medium. OK-432 (Chugai Pharmaceutical Co., Ltd., Tokyo) was added to this preparation and incubated for one to 4 days. Thereafter interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and interferon-gamma (IFN-gamma) levels in the culture supernatant were measured using enzyme-linked immunoassay kits. Cytokine production levels in cultures with OK-432 were significantly increased in the mononuclear cells of both patients and healthy volunteers. The largest increase was observed with IFN-gamma (p < 0.01), and then with IL-1 beta (p < 0.05). Responses of the cells from chronic hepatitis Type C patients to OK-432 were relatively good. When interferon (alpha and beta) treatment was first introduced, there were high hopes for a high efficacy. However, we now know 50-70% of patients with chronic hepatitis Type C do not respond satisfactorily to interferon. Some physicians suggest the necessity of using biological response modifier (BRM) as an adjuvant treatment for these patients. From our findings, OK-432 could be a useful BRM in patients with chronic hepatitis Type C.
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PMID:Effects of the streptococcal preparation OK-432 on in vitro cytokine production of peripheral blood mononuclear cells in patients with chronic viral hepatitis. 134 50

A 49-yr-old man with chronic hepatitis B manifested hypergammaglobulinemia, lymphadenopathy, and a high serum interleukin-6 level following treatment with recombinant human alpha-interferon. One month later, when the patient was treated with natural beta-interferon, serum levels of interleukin-6 and gamma-globulin increased again. The serum gamma-globulin decreased to the pretreatment level after discontinuation of interferon therapy. The serum alanine aminotransferase level remained normal for 6 months. In this case, hypergammaglobulinemia and lymphadenopathy, as well as the elevated serum interleukin-6 level, were considered to be signs of highly enhanced humoral immunity related to alpha- and beta-interferon therapy.
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PMID:Elevated interleukin-6 and gamma-globulin during interferon therapy of hepatitis B. 138 10

In previous reports we described our approach to the cultivation of murine and human thymic epithelial cells in primary cultures, using defined, serum-free growth factor-supplemented medium and extracellular matrix-coated culture plates. The cells in these cultures displayed high metabolic activity and their supernatant was highly active on thymocytes. In the study reported here we analysed cytokine activities in the supernatant of human thymic epithelial cell cultures (HTES), by using the respective cytokine-dependent cell lines and by neutralization with specific monoclonal antibodies. Three cytokine activities were detected--interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and macrophage (M)-CSF. Other cytokine activities tested for [IL-1, IL-2, IL-7, interferon (IFN) and tumour necrosis factor (TNF)] were negative. The effect of HTES on concanavalin A (Con A)-induced proliferation of murine thymocytes could be completely abolished by anti-IL-6 antibodies, but not by antibodies to CSF, whereas enhancement of bone marrow cell proliferation by HTES was partially inhibited by either anti-G-CSF or anti-M-CSF antibodies and completely inhibited by both antibodies, but not at all by anti-IL-6. We can thus distinguish between thymocyte-related cytokines (IL-6) and bone marrow (myeloid/monocyte) related ones (G-CSF, M-CSF) in HTES.
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PMID:Analysis of thymic stromal cell subpopulations grown in vitro on extracellular matrix in defined medium. IV. Cytokines secreted by human thymic epithelial cells in culture and their activities on murine thymocytes and bone marrow cells. 138 12

Interleukin-6 (IL-6) is a pleiotropic cytokine which produces uveitis if administered intraocularly. It has been demonstrated in the aqueous of patients with various uveitis entities. We have investigated the ability of human retinal pigment epithelium (RPE) to produce IL-6 in vitro, both unstimulated, and in the presence of interleukin-1 (IL-1), tumor necrosis factor alpha (TNF), interferon (IFN) gamma, and lipopolysaccharide (LPS). Five human RPE cell lines were cultured over a 6-day period, both unstimulated and in the presence of these cyokines. IL-6 in the supernatants was measured using an ELISA assay. Unstimulated RPE produced small amounts of IL-6. IL-1 at 100 or 10 U/ml markedly upregulated IL-6 production, and TNF at 1000, 100 or 10 U/ml did so to a lesser extent. Neither IFN gamma or LPS alone increased IL-6 expression, but together gave significant upregulation. Thus human RPE can produce IL-6 and may be the source of this cytokine in ocular inflammatory states.
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PMID:Production of interleukin-6 by human retinal pigment epithelium in vitro and its regulation by other cytokines. 142 42

Tumor necrosis factor and related cytokines are thought to be implicated in cell-mediated immunity and pathophysiology in malaria, but their mechanism of action has not been ascertained. Tumor necrosis factor has been reported to generate nitric oxide in vitro, so we have measured levels of this molecule and its products in the plasma of mice after they have received an injection of tumor necrosis factor, lymphotoxin, interleukin-1, gamma interferon, or interleukin-6, all of which have been reported to be increased in malaria. Total reactive nitrogen intermediate levels in plasma were assayed spectrophotometrically after exposing plasma to a copper-cadmium-zinc catalyst to convert nitrate to nitrite and then to Griess reagent. Tumor necrosis factor, lymphotoxin, and interleukin-1 all induced reactive nitrogen intermediates in vivo, with interleukin-1 showing the most activity. Tumor necrosis factor was then examined more closely. It induced more reactive nitrogen intermediates in malaria-infected mice than in normal mice, and appreciably more was in the form of nitrate than was in the form of nitrite. NG-methyl-L-arginine inhibited the in vivo generation of reactive nitrogen intermediates by tumor necrosis factor in a dose-dependent manner, implying that these molecules were arginine derived. These results are consistent with the possibility that tumor necrosis factor, lymphotoxin, and interleukin-1 may contribute to host pathology and parasite suppression through generation of nitric oxide.
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PMID:In vivo induction of nitrite and nitrate by tumor necrosis factor, lymphotoxin, and interleukin-1: possible roles in malaria. 150 Jan 82

The treatment of keloids in black patients remains a medical dilemma. Previous studies have focused on primary alterations in the metabolism of fibroblasts as the key in the etiology of this condition. Yet alterations in the production of various cytokines which may alter fibroblast responses secondarily have received little attention. Twelve black patients with clinical and histological diagnosis of keloids and eight black control volunteers were studied. Peripheral blood mononuclear-cell (PBMC) fractions from both groups were assayed for production of interleukin-1 (IL-1), interleukin-2 (IL-2), interleukin-6 (IL-6), alpha-interferon (IFN-alpha), beta-interferon (IFN-beta), gamma-interferon (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and tumor necrosis factor-beta (TNF-beta). The production of IFN-alpha, IFN-gamma, and TNF-beta were markedly depressed in keloid patients compared to normal controls. However, IL-1 and IL-2 production was not significantly different between the two groups. In contradistinction, keloid patients produce greater amounts of IL-6, TNF-alpha, and IFN-beta. Altered levels of immunoregulatory cytokines may play a significant role in the net increase in collagen which characterizes keloid formation.
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PMID:Altered cytokine production in black patients with keloids. 151 3


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