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)

Interleukin-6 (IL-6) is a cytokine produced by a number of cells, including macrophages, and is directly involved in the inflammatory response. The production of IL-6 can be stimulated by monokines such as IL-1 and tumor necrosis factor (TNF). Mycobacterium avium complex organisms frequently cause disseminated disease in patients with AIDS. M. avium is an intracellular bacterium that that mainly infects macrophages. Treatment of M. avium-infected macrophage monolayers with recombinant IL-6 decreased the ability of TNF to activate cultured macrophages to inhibit growth of or kill intracellular M. avium (68% +/- 14% decrease in intracellular killing compared with that in monolayers not treated with IL-6). To further evaluate whether this effect was dependent on the down regulation of membrane receptors to TNF, we examined 125I-TNF binding to macrophages previously exposed to IL-6: the expression of TNF receptors was decreased by 78% +/- 9%. The effect of IL-6 on TNF receptors was observed after 4 h and was reversible. Infection of macrophages with different M. avium serovars was associated with release of IL-6, and IL-6 production peaked at 48 h after infection in concentrations ranging from 328 +/- 87 ng/10(5) cells to 907 +/- 224 ng/10(5) cells. IL-6 did not have any influence on the rate of growth of the tested strains of M. avium within or outside macrophages. These results suggest that release of IL-6 by M. avium-infected macrophages may influence the host's immune response and the outcome of the disease.
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PMID:Interleukin-6 antagonizes tumor necrosis factor-mediated mycobacteriostatic and mycobactericidal activities in macrophages. 132 56

Infection with the human immunodeficiency virus-1 is associated with a marked increase in the incidence of Kaposi's sarcoma. Recent studies suggest that the risk of Kaposi's sarcoma in human immunodeficiency virus infection is increased with oral-fecal contact and that a sexually transmitted agent possibly related to human papillomavirus-16 could be involved. Exposure to this or another sexually transmitted agent apparently alters both the morphology and growth regulation of the Kaposi's sarcoma progenitor cells. These changes include the expression of the alpha chain of the interleukin-6 receptor with the acquisition of an interleukin-6-dependent autocrine growth loop. Subsequent perturbation of multiple cytokines during human immunodeficiency virus infection, including Oncostatin-M, interleukin-1 beta and tumor necrosis factor-alpha alters the subsequent growth of Kaposi's sarcoma. These studies suggest that control of cytokine perturbations or the underlying human immunodeficiency virus-1 infection should result in a significant reduction in the rate of growth of acquired immunodeficiency syndrome-related Kaposi's sarcoma.
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PMID:Pathogenesis of human immunodeficiency virus-related Kaposi's sarcoma. 133 10

To investigate a possible role of cytokines in parvovirus-mediated suppression of tumorigenesis, we tested in cell culture whether parvoviruses are able to induce interferon (IFN)-beta, tumor necrosis factor (TNF)-alpha or interleukin-6 (IL-6). Infection of rodent or human cells with the parvoviruses minute virus of mice (MVM), H-1 or adeno-associated virus (AAV) types 2 or 5 failed to induce expression of the luciferase or beta-galactosidase reporter genes transfected into these cells as constructs containing an IFN-beta promoter. Parvoviruses did weakly induce synthesis of TNF-alpha and of IL-6 in cell culture and could slightly enhance synthesis of these cytokines when induced by other agents. These in vitro data suggest that the rather unspecific tumor-suppressive properties of parvoviruses are unlikely to be attributable to stimulation of the synthesis of IFN, TNF or IL-6.
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PMID:Parvoviruses are inefficient in inducing interferon-beta, tumor necrosis factor-alpha, or interleukin-6 in mammalian cells. 152 25

Studies on intraabdominal infections have been difficult to compare in the past due to a missing system of classification for peritonitis. According to a recently developed classification system, secondary peritonitis, including spontaneous acute peritonitis, postoperative peritonitis and posttraumatic peritonitis, is the most common complication of severe intraabdominal infections. In several studies the mortality rate of postoperative peritonitis was still between 60% and 79%. Scoring systems were developed, some of them with the idea to predict mortality in peritonitis. Although the APACHE II score cannot predict the outcome of peritonitis in an individual patient, it is a reliable, valid and objective system for risk stratification in intraabdominal infections. Local trauma or bacterial contamination is responsible for an acute phase reaction, which involves the release of certain cytokines such as TNF-alpha, interleukin-1 (IL-1) and interleukin-6 (IL-6). The IL-6 seems to play an important role in the mechanism of the acute phase reaction, acting on hepatocytes to release acute phase proteins (e.g. CRP). Preliminary results of investigations of IL-6 levels in peritonitis indicate a possible role for IL-6 as a predictor of the outcome of peritonitis.
Infection
PMID:Intraabdominal infections: classification, mortality, scoring and pathophysiology. 181 19

Infections by gram-negative bacteria are one of the major causes of death in newborns. Bacterial clearance is deficient in septic neonates, which seems to increase their susceptibility to infections. In this study, we observed a significant improvement in clearance of Klebsiella pneumoniae in newborn wistar rats inoculated by intraperitoneal via with 800 mg k soybean phosphatidylcholine (PC), compared to the control group injected with PBS (p 0.05). The overall survival rate was improved (p 0.05) and the white blood cell counts showed a greater leukocytosis and neutrophilia during the peak of bacteremia in the PC treated animals. Circulating levels of interleukin-6 were greater in the PC group, which developed an intense splenic hematopoiesis of the granulocyte (p 0.05) and megakariocyte series (p 0.01). No significant changes were observed in bone marrow granulocyte deposits in both study groups. The improvement in survival rate, the changes in leukocyte counts and the splenic hematopoiesis may be associated with the increased production of IL-6. These results suggest that IL-6 plays a role in the protection mechanism induced by PC in this experimental model of newborn septicemia. PC seems to be an immunomodulator of the acute response to gram-negative bacterial infection.
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PMID:[Phosphatidylcholine induces an increase in the production of interleukin-6 and improves survival of rats with neonatal sepsis caused by Klebsiella pneumoniae]. 749 35

Cytokines, especially tumor necrosis factor alpha (TNF alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) play an important role in the genesis and progression of the septic shock syndrome. We performed a study monitoring levels of these three cytokines in ten neutropenic oncology patients in whom an infectious syndrome was suspected. A comparison was made with a population of nine non-neutropenic patients on the intensive care unit. Unfortunately the results of this study do not allow specific profiles to be established for each cytokine in the populations studied. Levels of IL-6, TNF alpha and IL-1 beta were not statistically higher in the non-neutropenic patients when compared with the neutropenic group. However, the highest IL-6 levels were observed for four non-neutropenic patients, three of whom died. High levels of C-reactive protein (CRP), haptoglobin and fibrinogen were found, reflecting the inflammatory status of each patient. CRP levels were higher in the non-neutropenic patients and correlated with IL-6 levels, indicating the importance of CRP determination in this group of patients.
Infection
PMID:TNF alpha, IL-1 beta and IL-6 plasma levels in neutropenic patients after onset of fever and correlation with the C-reactive protein (CRP) kinetic values. 753 Nov 79

Infection with cytomegalovirus (CMV) continues to be one of the most common complications following allogeneic bone marrow transplantation. The gravest danger for the host occurs when the virus is reactivated as a result of immunosuppression. In this report we studied the effects of sublethal murine cytomegalovirus (MCMV) infection on the hemopoietic system including bone marrow (BM) cellularity, production of colony stimulating factor (CSF) and interleukin-6 (IL-6) and the development of granulocyte-macrophage colony forming units (CFU-GM), and BM stromal cell viability. Our findings show that the virus infection led to a significant decrease in the number of BM cells and in the production levels of CSF and IL-6. There was also a decrease in the number of stromal cells, as reflected by the number of colony forming unit fibroblasts (CFU-F), and in the relative number of CFU-GM progenitors. Treatment of MCMV infected mice with the immunomodulator AS101 [ammonium trichloro (dioxyethylene 0-0')tellurate] restored significantly CSF and IL-6 production by BM cells to levels of uninfected control mice as well as the number of CFU-F and stromal cell elements which consequently led to the restoration of the total number of BM cells. Results presented here indicate that AS101 may have immunomodulatory effects on MCMV mediated myelosuppression. Administration of AS101 to patients with CMV associated BM damage may improve the restoration of their BM function.
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PMID:Restoration of murine cytomegalovirus (MCMV) induced myelosuppression by AS101. 772 28

Infections, trauma and inflammatory processes induce a host response with increases in a large group of structurally and functionally diverse plasma proteins. Parental administration of foreign proteins also induce an increase in plasma fibrinogen. Interleukin-6 (IL-6) is a monocyte-derived mediator and has regulatory effects on acute phase protein genes which result in the induction of fibrinogen synthesis in primary hepatocytes, while the addition of interleukin-1 (IL-1) exerts a negative modulating influence on the IL-6-stimulated fibrinogen. In order to understand the mechanisms by which IL-1 inhibits IL-6-stimulated fibrinogen transcription and translation, and since IL-1 is believed to act through PGE2 stimulation, we have studied the influence of PGE2 in IL-6 or IL-1, alone and in combination, on Fg mRNA expression (by Northern blot analysis) and the influence of PGE2, indomethacin, and arachidonic acid on Fg secretion. Moreover, since human recombinant interleukin-1 receptor antagonist (hrIL-1ra) is a strong inhibitor of IL-1 induced IL-1 transcription and translation and has an inhibitory effect on PGE2, we have studied the effects of IL-1ra on the down-regulation of IL-6 stimulated fibrinogen by IL-1, using an Fg ELISA method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The down-regulation of IL-6-stimulated fibrinogen steady state mRNA and protein levels by human recombinant IL-1 is not PGE2-dependent: effects of IL-1 receptor antagonist (IL-1RA). 777 69

This study was designed to investigate serum soluble interleukin-2 receptor (S-IL-2R), interleukin-2 (IL-2) and interleukin-6 levels (IL-6) in patients with either a positive or negative Borrelia burgdorferi serology. Serum samples from 101 individuals, divided in to five groups according to clinical symptoms and outcome of serology were analysed. Samples of cerebrospinal fluid (CSF) from nine of the individuals were also studied. The highest average serum S-IL-2R levels (1,180 +/- 1,140 U/ml) were found in patients with erythema migrans, the hallmark of Lyme borreliosis, followed by patients with symptoms closely related to Borrelia infection (900 +/- 1,200 U/ml) and with a strong positive serology. In two patients with central nervous system (CNS) involvement, increased levels of S-IL-2R of 920 and 620 U/ml respectively (normal value < 50 U/ml) were detected in the CSF. No statistically significant relationship between IgG or IgM antibody activity and serum S-IL-2R levels was found. Detectable levels of IL-2 were only found in three patients. Increased levels of IL-6 were found in sera from 14 patients. The highest concentration, 90 pg/ml (normal value < 10 pg/ml), was measured in a patient presenting with vasculitis. In conclusion, B. burgdorferi infection causes a moderate increase of serum S-IL-2R levels, although there is no relationship between the severity of the infection, as estimated by the antibody concentration or to serum IL-2 or IL-6 levels. Secondary complications of the infection, such as vasculitis, may cause an increased level of serum IL-6.(ABSTRACT TRUNCATED AT 250 WORDS)
Infection
PMID:Response of soluble IL-2 receptor, interleukin-2 and interleukin-6 in patients with positive and negative Borrelia burgdorferi serology. 784 8

1. Infection in the neonatal period is difficult to diagnose and is a significant cause of morbidity and mortality in preterm infants. 2. We investigated prospectively the predictive value of plasma measurement of bacterial endotoxin (lipopolysaccharide), tumour necrosis factor-alpha, interleukin-6, interleukin-8, intercellular adhesion molecule-1 and C-reactive protein in 60 consecutive newborn infants suspected of having neonatal infection. Plasma samples were taken at the time of acute clinical deterioration. Sixty-two cord blood samples were studied as controls taken at elective Caesarean section. 3. Forty-three infants had confirmed infections, 25 with positive blood cultures. Tumour necrosis factor-alpha and bacterial endotoxin levels were not significantly elevated over controls, whereas interleukin-6, interleukin-8 and intercellular adhesion molecule-1 levels were all significantly increased in the infected group compared with controls (all P < 0.001). 4. Increased plasma intercellular adhesion molecule-1 levels were a highly sensitive (88%) indicator of clinical infection and were independent of C-reactive protein. Use of these two assays in combination improved the diagnostic sensitivity to 95% and gave a negative predictive value of 97%. addition of interleukin-6 or interleukin-8 measurements failed to further significantly enhance the prediction of infection. 5. Measurement of intercellular adhesion molecule-1 level may have a clinical role in rapidly confirming, or predicting, the likely diagnosis in cases of suspected neonatal infection.
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PMID:Predictive value of soluble immunological mediators in neonatal infection. 792 61


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