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

Our objective was to determine the incidence of peritonitis episodes with an impaired initial cell reaction (IICR:neutrophil number < 100 x 10(6)/L) over a period of ten years, and to find possible explanations for this unusual presentation of peritonitis. A retrospective review of the files of continuous ambulatory peritoneal dialysis (CAPD) patients included in the CAPD program 1984 and 1993 was done. Analysis of cytokine and prostanoid patterns during four peritonitis episodes with an IICR was compared to 12 episodes with a normal initial cell reaction (NICR). Dialysate cell numbers and immunoeffector characteristics of peritoneal cells were compared in 7 IICR patients in a stable situation and a control group of 70 stable CAPD patients. The setting was a CAPD unit in the Academic Medical Center in Amsterdam. Thirty-five CAPD patients who had one or more peritonitis episodes with an IICR and a control group of 249 CAPD patients were included in the study. The incidence of peritonitis with an IICR was 6%. These episodes occurred more than once in 51% of the patients who presented with IICR. In 72% the cell reaction was only delayed: a cell number exceeding 100 x 10(6)/L was reached later. Staphylococcus aureus was significantly more frequently the causative microorganism compared to all peritonitis episodes (PE) that occurred during the study period. Patients with IICR had lower dialysate cell counts in a stable situation, compared to a control group (p < 0.01). This was caused by a lower number of macrophages and CD4 positive lymphocytes. The phagocytosis capacity of the macrophages appeared to be normal. In a comparison of four PE with an IICR and 12 episodes with an NICR, the tumor necrosis factor-alpha (TNF-alpha) response was similar and occurred on day 1, also pointing to normally functioning macrophages. However, the maximal appearance rates of interleukin-6 (IL-6) and IL-8 occurred later in the episodes with IICR compared to NICR (day 2 vs day 1, p < 0.05). No differences were found in vasodilating prostaglandins, mesothelial cell markers (cancer antigen 125, phospholipids, hyaluronan), and mesothelial cell numbers in the stable situation nor during peritonitis. Peritonitis can present as abdominal pain in the absence of a cloudy dialysate. In some of the patients this presentation occurred more than once. This impaired, most often delayed, cell reaction was associated with a delayed secondary cytokine response. As IL-6 and IL-8 can be synthesized by mesothelial cells, this suggests an impaired functioning mesothelium. This could not be confirmed, however, by a lower number of mesothelial cells in effluent or lower dialysate levels of mesothelial cell markers.
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PMID:Impaired initial cell reaction in CAPD-related peritonitis. 872 24

This study was designed to investigate changes in the immune system of elite swimmers compared with well-conditioned age- and sex-matched controls in relation to a competition swim (field study). Furthermore, the aim was to reveal possible differences in immune system changes depending on the type of sport performed by comparing with an earlier study of similar design, from the same laboratory that tested elite runners in relation to a competition run. The swimmers were tested before, immediately after and 2 h and 24 h after a competition swim. Lymphocyte subsets (CD5, CD3, HLA-DR, CD4, CD8, CD19, CD3/CD16+56, CD57, CD18, CD16/CD122) all increased after the run, decreased to normal or subnormal levels after 2 h, and returned to normal after 24 h (absolute numbers). The findings were identical for the swimmers and the age- and sex-matched control group. No change in polymorphonuclear granulocyte migration was found. The lymphocyte proliferative responses decreased 2 h after the exercise. No changes were seen in plasma cytokine levels (interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) in relation to exercise, but significantly lower baseline values for IL-6 were observed in the swimmers. An increase in total natural killer cell activity immediately after exercise, followed after 2 h by a decrease, was seen in both swimmers and controls. Finally, no complement activation was detected. Compared with an earlier study of elite runners, differences were seen in granulocyte chemotactic response, TNF-alpha plasma activity and the lymphocyte proliferative response to mitogen. These differences might be explained by the degree of immune system activation following muscle damage during exercise, inducing an increase in cytokines, which are known to activate and modulate both lymphocytes and granulocyte function. Our findings demonstrate identical exercise-induced, immune system changes in elite swimmers and well conditioned controls, and furthermore, the findings suggest that different types of sport performed at maximum intensity induce different immune system changes.
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PMID:Short-term changes in the immune system of elite swimmers under competition conditions. Different immunomodulation induced by various types of sport. 882 44

A 57-year-old female was admitted to Uji hospital for the further evaluation of nodular shadow on her right lung. During the period of admission, she developed cervical lymph node swelling. She was diagnosed as having malignant lymphoma (diffuse, small cleaved cell) by lymph node biopsy. She received combined chemotherapy and obtained partial remission for seven months until she developed fever and pancytopenia. Laboratory data showed increased number of large granular lymphocytes (LGLs) in blood. Bone marrow revealed increased number of LGLs with hemophagocytosis by macrophage. Surface marker analysis revealed LGLs were positive for CD2 CD16, and CD56 and negative for CD3, CD4, CD8, and CD20. T-cell receptor genes beta and gamma were in germ line configuration. Analysis of Epstein-Barr virus genome using termini probe indicated a monoclonal proliferation of LGLs. Reexamination of the biopsy specimen of lymph node revealed LGLs which was negative for CD3 and CD20. The patient was diagnosed as a leukemic phase of natural killer (NK) cell lymphoma complicated with hemophagocytic syndrome (HPS). Serum levels of interferon-gamma, macrophage colony-stimulating factor, granulocyte colony-stimulating factor, and interleukin-6 increased, which might be related to HPS.
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PMID:[Natural killer cell lymphoma having a nodular shadow in the lung as an initial finding, developed to leukemia complicated with hemophagocytic syndrome at the time of relapse]. 882 78

Interferon-alpha combined with retinoid or PUVA is used for the treatment of cutaneous T-cell lymphoma. Anti-IFN-alpha antibodies (IFN ab) occur regularly during IFN-alpha treatment. We investigated the incidence of neutralizing and binding IFN ab and analysed their relationship with clinical and immunological parameters. A group of 17 CTCL patients were treated with IFN alpha-2a three times weekly subcutaneously at a dose of 3 Mill. I.U. combined either with retinoid (acitretin, Neotigason; 0.5 mg/kg bodyweight) daily or with 5-methoxypsoralen (1.2 mg/kg bodyweight) plus UVA radiation three times weekly. Prior to and during treatment we monitored stage, skin involvement by a tumour burden index, serum levels of beta 2-microglobulin, neopterin, binding and neutralizing IFN ab, Interleukin-6 (IL-6), soluble IL-2 receptors (sIL-2r) and the CD4/CD8 ratio of peripheral blood mononuclear cells. We observed two complete, two partial and six minor responses, four patients with stable disease and three patients with progressive disease. Of the 17 patients, 7 developed binding IFN ab, but only 2 had neutralizing IFN ab which were associated with high titres of binding IFN ab. IFN ab formation was more frequent in patients with normal CD4/CD8 ratios and a high tumour burden index and showed a trend to be more frequent in PUVA-cotreated patients than in retinoid-cotreated patients. Responses were more frequently seen in IFN ab-negative patients. IFN ab developed in patients treated with PUVA or retinoid combined with IFN. Binding as well as neutralizing IFN ab may have an impact on the treatment success in CTCL patients.
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PMID:Incidence and in-vivo relevance of anti-interferon antibodies during treatment of low-grade cutaneous T-cell lymphomas with interferon alpha-2a combined with acitretin or PUVA. 887 50

Interleukin-6 (IL-6) is a cytokine with pleiotropic biologic activities on B cells, T cells, and hematopoietic progenitors. The present study was undertaken to assess pharmacodynamic effects of subcutaneous administration of IL-6 on blood counts, immunologic parameters, and acute-phase reactants. Blood samples were taken from patients with advanced renal cell cancer participating in a phase II trial of recombinant human IL-6. Multiparameter FACS analyses of peripheral blood mononuclear cells were performed using antibodies against CD3, CD4, CD8, HLA-DR, CD56, CD28, CD38, CD19, sIgM, and sIgG. Serum levels of IL-10, soluble CD23 (sCD23), sCD25, IL-1 receptor antagonist protein (IL-1RA), soluble tumor necrosis factor (TNF) receptors (sTNF-R) p55 and p75, and soluble IL-6 receptor (sIL-6R) were detected by ELISA systems. Levels of C-reactive protein (CRP), neopterin, fibrinogen, beta 2-microglobulin, and immunoglobulins M, G, and A were measured by standard methods. In response to administration of IL-6, a significant increment in platelet counts was observed, reaching peak levels after 21 days of treatment. In contrast, leukocyte subsets remained unaffected. No change in number of immunophenotype of peripheral blood B cells, T cells, or natural killer cells could be detected following IL-6 administration. Blood levels of sCD23, IL-10, sIL-6R, neopterin, beta 2-microglobulin, and immunoglobulin subsets were not influenced by cytokine therapy. However, administration of IL-6 led to a slow increment of acute-phase reactants CRP and fibrinogen. Furthermore, the anti-inflammatory molecules sTNF-R p55 and p75 were induced by IL-6, whereas serum levels of IL-1RA remained unchanged. Finally, an increase in blood levels of sCD25 was observed. In conclusion, IL-6 in vivo predominantly acts as a regulator of inflammation and a megakaryocyte differentiation factor.
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PMID:Immunomodulatory and hematopoietic effects of recombinant human interleukin-6 in patients with advanced renal cell cancer. 893 65

Interleukin-6 (IL-6) and Interferon gamma (IFN-gamma) production was analyzed in mice after topical exposure of the animals to Oxazolone, a well-known contact sensitizer. Since both IL-6 and IFN-gamma had been shown to be involved in the initiation of delayed-type hypersensitivity (DTH) reactions, and especially in contact sensitization (CS), we focussed our analysis on the cellular source of the two cytokines in local lymph nodes draining the site of exposure. We have demonstrated that IL-6 is found exclusively in lymph node antigen presenting cells (LNAPC), using three different approaches: i) in vitro restimulation of CD4-positive cells, obtained from Oxazolone-treated mice, in the presence of I-A-positive LNAPC, led to a strong IL-6 response, measured in culture supernatants by ELISA. Depletion of LNAPC in these suspensions prior to cultivation diminished IL-6 secretion, indicating that the LNAPC were the sole source of IL-6, ii) Staining of restimulated LNC for intracellular cytokines confirmed that LNAPC are the only source of IL-6 at various time-points during cultivation. iii) Competitive PCR analysis of cDNA, derived from freshly isolated lymph node cells (LNC) depleted either in CD8/B220- or CD8/B220/I-A-positive cells, showed that ex vivo IL-6-specific mRNA was found exclusively in the LNAPC. In contrast IFN-gamma is produced by CD4+ cells, although in some experiments CD8+ cells were also positive. Time-course analysis of the secretion of the two cytokines and their relation to lymphocyte blastosis in vitro showed that IL-6 peaked during the first 6 hrs of restimulation, whereas the number of IFN-gamma producing cells reached a maximum after 24 hrs and were closely correlated with the increasing number of in vitro blastocytes. Our data corroborate with other authors' investigations of DTH reactions, showing that IL-6, provided by LNAPC during primary responses in vivo, may serve as a co-stimulating factor for T cells.
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PMID:Murine lymph node antigen presenting cells are the main source of interleukin-6 in the initiation of delayed-type hypersensitivity. 895 84

The effects Lactobacillus casei YIT9108 (LC 9018) on antitumor activity and cytokine production in Meth A fibrosarcoma (Meth A)-bearing BALB/c mice were examined. Intrapleural (i.pl.) administration of LC 9018 was effective in prolonging the survival of Meth A-bearing mice, and frequently cured mice of the tumor. However, the results also indicated that the effect of LC 9018 was in part inhibited in mice treated with anti-CD3 or anti-CD8 antibody, but not affected in anti-CD4 antibody-treated mice. In contrast, LC 9018 had little effect on Meth A-bearing SCID or nude mice. These results demonstrated that CD8+ T cells participated in prolonging the survival of Meth A-bearing mice. Moreover, the examination of the production of several cytokines revealed that the production of interferon-gamma and interleukin-6 was, in particular, augmented in the exudated fluid of the thoracic cavity in BALB/c mice injected with LC 9018 i.pl. These results suggested that i.pl. administration of LC 9018 induced those cytokines which had the potential to activate the thoracic macrophages or proliferate the thoracic lymphocytes to the cytotoxic T cells. Taken together, these findings demonstrated that the prolonging effects on survival by i.pl. administration of LC 9018 depended on CD8+ T cells, and the i.pl. administration of LC 9018 into i.pl. Meth A-bearing mice induced several cytokines which participated in the subsequent immunoresponses.
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PMID:Effects on antitumor activity and cytokine production in the thoracic cavity by intrapleural administration of Lactobacillus casei in tumor-bearing mice. 900 21

The role of mononuclear phagocytes and their cytokine products in host defense against Pneumocystis carinii (PC) remains unclear. The cytokine tumor necrosis factor (TNF) has been proposed as critical for host defense against this pathogen. To investigate the role of this cytokine in PC infection, we treated immunocompetent mice (CD4+) or mice depleted of CD4 lymphocytes (CD4-) with a recombinant adenovirus encoding a TNF inhibitor gene (AdTNF-R). AdTNF-R treated CD4+ animals displayed delayed clearance of PC after intratracheal inoculation, whereas AdTNF-R treated CD4 animals developed more severe chronic infection. Moreover, AdTNF-R treated CD4- animals, in contrast to control CD4- mice, failed to show any interleukin-6 (IL-6) gene induction in the lung after PC challenge. The results firmly implicate TNF in host defense against PC, and support a role for TNF in orchestrating the intrapulmonary cytokine cascade in PC infection.
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PMID:Exacerbation of murine Pneumocystis carinii infection by adenoviral-mediated gene transfer of a TNF inhibitor. 903 17

In this study we compared cytokine production and cell proliferation of immunocompetent cells derived from patients with ankylosing spondylitis (AS) to those from healthy blood donors using a whole blood assay. To this end, blood cell cultures were stimulated with the superantigens MAS (Mycoplasma arthritidis supernatant) and staphylococcal enterotoxin B (SEB) and the plant lectins phytohaemagglutinin (PHA) and concanavalin A (Con A). The number of white blood cells (WBC) and lymphocyte subsets were also determined. Cell proliferation and levels of interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) were measured after stimulation with the different mitogens. An ELISA test was used to analyse supernatant cytokine levels. Individuals with AS showed significantly lower IFN-gamma concentrations and markedly lower cell proliferation rates with all tested mitogens than healthy controls, while there was no significant difference in IL-6 synthesis. IL-1 beta levels were slightly impaired in the patient group, but only blood cell cultures stimulates with MAS showed a statistical significance. Furthermore, there was a significant elevation of leucocytes and lymphocytes in patients with AS resulting in higher numbers of CD4-positive cells, which implies a higher CD4:CD8 cell ratio. CD19- and CD8-positive cells were not significantly distinct compared to healthy controls. This deviation in cytokine levels and cell proliferation points to a suppression of T lymphocytes. A disturbed T-lymphocyte function may play a part in the pathogenesis of AS.
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PMID:Stimulation of whole blood cultures in patients with ankylosing spondylitis by a mitogen derived from Mycoplasma arthritidis (MAS) and other mitogens. 903 20

Synovial fluid samples from 21 rheumatoid arthritis patients were analyzed for lymphocyte subsets using flow cytometry and antibodies to the lymphocyte surface antigens CD3, CD4, CD8, CD16, CD19, CD29, and CD45RA. Synovial fluid levels of interleukin-6, rheumatoid factors and acute phase proteins were also measured. Depletion of CD45RA+ cells and predominance of CD29+ cells were found. Interleukin-6 levels were markedly elevated (1155 pg/ml; range, 24-3875 pg/ml), as were levels of IgM, IgG and IgA rheumatoid factors and of acute phase proteins. CD4 + CD29+ counts were significantly correlated with interleukin-6 levels. Interleukin-6 levels were significantly correlated with levels of all three rheumatoid factor classes but not with levels of acute phase proteins. Significant correlations were also found between CD19+ B counts and levels of all three rheumatoid factor classes. These data suggest that synovial fluid CD4 + CD29+ cells may be involved in the immune dysregulation characteristic of rheumatoid arthritis. The correlation between CD4 + CD29+ counts and interleukin-6 levels is consistent with the recent hypothesis that, together with monocytes, CD4 + CD29+ cells are an important source of the elevated levels of interleukin-6 seen in rheumatoid synovial fluid.
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PMID:Relations between absolute number of CD4 + CD29+ memory cells and levels of interleukin-6, rheumatoid factors, and acute phase proteins in rheumatoid synovial fluid. 909 Jul 64


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