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)

The relationship among "negative" plasma acute-phase proteins (APP), ie, albumin, prealbumin, and transferrin, and "positive" APP, ie, C-reactive protein (CRP), fibrinogen, and orosomucoid, was investigated in patients with acute infectious disease (n = 8) and in patients with chronic malignant disease (n = 9). In addition, the transcapillary escape rate (TER) and outflux (J(alb)) of albumin were investigated using an intravenous injection of 2 microCi 125I-albumin. Interleukin-6 (IL-6) plasma concentrations were measured with an enzyme immunoassay. In the majority of patients, negative APP were decreased, whereas positive APP were increased. However, in patients with infectious disease, there were no significant correlations between any of the negative and positive APP. Also, in patients with infectious disease, TER was increased to 8.6 +/- 3.4%/h (mean +/- SD), and J(alb) to 114 +/- 60 mg/kg/h, compared with normal values of 4.3 +/- 2.6%/h and 108 +/- 7 mg/kg/h, respectively. Unexpectedly, there was a significant positive correlation between plasma albumin and both TER (r = .8279, P = .011) and J(alb) (r = .8683, P = .005). In patients with malignomas, significant correlations within negative and positive APP and inverse correlations between negative and positive APP resulted. Malignant disease induced only a slight elevation in TER (6.6 +/- 2.4%/h), J(alb) was within normal limits (92 +/- 35 mg/kg/h), and no correlations between plasma albumin concentrations and TER (r = -.0174, P = .97) or J(alb) (r = .4090, P = .27) were found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transcapillary escape rate of albumin positively correlates with plasma albumin concentration in acute but not in chronic inflammatory disease. 751 58

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

We have produced interleukin-6 (IL-6)-deficient mice to examine, in vivo, the wide variety of biological activities attributed to this multifunctional cytokine. To investigate the role of IL-6 during infectious disease, IL-6-deficient mice were challenged with sublethal doses of Listeria monocytogenes, a facultative intracellular bacterium. While normal control animals were able to clear the infection, mutant animals exhibited a high mortality rate and showed uncontrolled replication of the bacteria in the spleen and liver at 2 and 3 days postinfection. Sections of infected tissues showed an increase in the number and severity of inflammatory foci. All aspects of this phenotype in the mutant animals were completely reverted upon administration of recombinant murine IL-6 (rIL-6). Various parameters of natural killer (NK) cell and macrophage function were unaffected in the challenge of the mutant animals. However, IL-6-deficient animals failed to mount peripheral blood neutrophilia in response to listeriosis, whereas control animals displayed a prominent neutrophilia in the blood at 24 and 48 h postinfection. Additionally, we analyzed the efficacy of rIL-6 in protecting animals devoid of lymphocytes or devoid of neutrophils during listeriosis. Administration of rIL-6 was protective to animals devoid of lymphocytes, suggesting that the rIL-6 protective effect was not mediated through lymphocytes. In contrast, control and mutant animals depleted of neutrophils were refractory to the rIL-6 protective effect. These data suggest that IL-6 is critical early during listeriosis, perhaps acting by stimulating neutrophils either directly or indirectly. Additionally, these data show a promising therapeutic potential for rIL-6 administration during opportunistic infection.
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PMID:Interleukin-6-deficient mice are highly susceptible to Listeria monocytogenes infection: correlation with inefficient neutrophilia. 776 7

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

Interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF) are important mediators of fever and inflammation, and are involved in the pathogenesis of sepsis. There is only limited data on serum concentrations of these proinflammatory cytokines in patients with fever and neutropenia, and their interrelationship and correlation with body temperature and clinical disease early in the febrile response during neutropenia have not been studied. Immunoreactive TNF, IL-1 beta, IL-6, and IL-8 in serum samples serially obtained from 14 adult patients with neutropenia and fever considered or documented to be due to infection were measured. IL-6 and Il-8 were consistently elevated in all patients, and correlated well with each other and with body temperature. Median peak concentration of IL-6 and IL-8 were 400 pg/ml (range: 100 to 41,000 pg/ml), and 1,025 pg/ml (range: 600 to 26,000 pg/ml), respectively, and levels of both cytokines rapidly declined in patients responding to antimicrobial therapy. Despite frequent sampling before and after the temperature peaks TNF and IL-1 beta, conversely, were less frequently detectable, with median peak values of < 10 pg/ml (range: < 10 to 150 pg/ml) for TNF, and 17 pg/ml (range: < 10 to 36 pg/ml) for IL-1 beta, respectively. The role of neutro- and monocytopenia with depletion of important cytokine producing and target cells in this particular cytokine response pattern needs to be further studied.
Infection
PMID:Kinetics and correlation with body temperature of circulating interleukin-6, interleukin-8, tumor necrosis factor alpha and interleukin-1 beta in patients with fever and neutropenia. 792 10

Serum levels of interferon gamma, interleukin-6 and neopterin were determined in 15 patients with different forms of Epstein-Barr virus-associated diseases: acute self-limiting infectious mononucleosis, chronic active infectious mononucleosis and X-linked lymphoproliferative syndrome. In patients with acute type of infection, neopterin, interferon gamma and interleukin-6 were elevated in nearly all patients. In contrast, the situation was less clear-cut in the other EBV-associated diseases; particularly interleukin-6 was undetectable in most cases. The results suggest that concomitant measurement of these diverse immune activation markers may provide interesting insights into the interactions between the virus and the host, and may also lead to therapeutic consequences.
Infection
PMID:Serum concentrations of interferon gamma, interleukin-6 and neopterin in patients with infectious mononucleosis and other Epstein-Barr virus-related lymphoproliferative diseases. 822 23

Tumor Necrosis Factor (TNF) is one of the many cytokines that comprise a complex intertwined network of biological response modifiers that takes on extreme significance as the host response to infectious diseases. Soluble factors such as Interleukin-2 and Interferon-gamma released by T cells and Interleukin-1, Interleukin-6 and TNF released by monocytes have been shown to play key roles in proliferation, activation and differentiation of immune cells. It has also become evident that development of treatment modalities for infectious diseases is complicated by the complexity of this cytokine network. In the last decade numerous reports have presented data, often conflicting, which clearly demonstrate a role for TNF in the response to infections caused by viruses. This review summarizes this rapidly growing volume of data, discussing consistencies and discrepancies as appropriate. By better understanding the role of TNF in the host immune response, it may be possible to modulate this complex network for the benefit of the host in its battle against viral infection.
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PMID:The role of tumor necrosis factor in viral disease. 827 14

Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.4 ng/kg body wt) intravenously on two separate occasions. Nocturnal sleep was recorded, and rectal temperature and the plasma levels of tumor necrosis factor-alpha, interleukin-6, adrenocorticotropic hormone, and cortisol were monitored for 12 h. Endotoxin reduced the relative amounts of wakefulness (P < 0.05) and rapid-eye-movement (REM) sleep (P < 0.05) and increased the relative amount of non-REM sleep (P < 0.01). Electroencephalogram delta power during non-REM sleep, as measured by spectral analysis, was not altered by endotoxin. The endotoxin-induced changes in sleep structure were related temporally and quantitatively to the increases in rectal temperature and to the release of cytokines and neurohormones. It is concluded that cytokines and neurohormones mediate the effects of endotoxin upon sleep. The ensuing increase in non-REM sleep may be part of the adaptive host response to bacterial infections in humans.
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PMID:Influence of endotoxin on nocturnal sleep in humans. 839 56


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