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)

This study compared the serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interferon gamma (IFN-gamma) in 78 Colombian patients, from two ethnic groups, with dengue virus infection. TNF-alpha levels were significantly higher in Afro-Colombians than in Mestizos and IL-6 levels were significantly higher in Mestizos than in Afro-Colombians, during the acute phase. IFN-gamma levels were similar in both ethnic groups. Significantly higher TNF-alpha levels were found in Afro-Colombians than in Mestizos in both dengue fever (DF) and dengue hemorrhagic fever (DHF). The IL-6 levels were higher in Mestizos than in Afro-Colombians among patients with DF, but levels of this cytokine were higher in Afro-Colombians than in Mestizos among patients with DHF. Levels of IFN-gamma were higher in patients with DHF than DF. Higher levels of these cytokines were observed in secondary infection. These results suggest that ethnicity may contribute to differences in immune responses to dengue infections.
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PMID:Serum levels of cytokines in two ethnic groups with dengue virus infection. 1898 2

Clinical features such as cough, sputum production, fever, and the presence of a new lung infiltrate seen on radiograph are not specific to respiratory tract infection, nor do they define the need for antibiotic therapy. Therefore, investigators have looked for biological markers that can supplement clinical information to determine whether the etiology of the infection is more likely bacterial, needing antibiotic therapy, or viral. There are studies of a number of biological markers in serum and bronchoalveolar lavage fluid, including cytokines, acute-phase reactants, and immunoglobulins. The 2 most promising markers in serum are C-reactive protein and procalcitonin (PCT). PCT is a hormokine, produced primarily by parenchymal cells in response to microbial toxins and in response to certain host inflammatory mediators (interleukin-1beta, tumor necrosis factor-alpha, and interleukin-6). Because PCT is down-regulated in the presence of viral infection, PCT seems most promising for defining the need for antibiotic therapy among patients with radiographic evidence of pneumonia. Studies using the highly sensitive Kryptor assay have shown that PCT guidance can lead to the safe withholding of antibiotics among patients with low PCT levels (<0.25 microg/L) and no clinical signs of severe illness. In addition, serial measurements of PCT have been reported to correlate with clinical response to therapy and may be able to guide short durations of therapy. In the future design of trials for community-acquired pneumonia, we may want to exclude patients with low PCT levels, because they are unlikely to benefit from antibiotic therapy. On the other hand, inclusion of patients with low PCT values creates heterogeneity in the study population and confounds the interpretation of clinical trial end points.
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PMID:Biological markers to determine eligibility in trials for community-acquired pneumonia: a focus on procalcitonin. 1898 78

Numerous Echinacea preparations are available on the market for the prevention and treatment of cold and 'flu symptoms and inflammatory conditions associated with infections. Most of these preparations are consumed orally in the form of aqueous or ethanol extracts and tinctures. Since the recommended consumption normally involves a brief local exposure to the diluted preparation at an unspecified time in relation to the actual infection, then it is important that experimental models for the evaluation of Echinacea reflect these limitations. A line of human bronchial epithelial cells, in which rhinoviruses stimulate the production of pro-inflammatory cytokines, was used to evaluate several relevant parameters. The chemically characterized Echinacea preparation (Echinaforce) was capable of inhibiting completely the rhinovirus induced secretion of IL-6 (interleukin-6) and IL-8 (chemokine CXCL-8) in these cells, regardless of whether the Echinacea was added before or after virus infection, and in response to a range of virus doses. This inhibitory effect was also manifest under conditions resembling normal consumption with respect to the duration of exposure to Echinacea and the Echinacea dilution. It is concluded that under real life conditions of Echinacea consumption, the virus-induced stimulation of pro-inflammatory cytokines can be effectively reversed or alleviated.
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PMID:Echinacea as an antiinflammatory agent: the influence of physiologically relevant parameters. 1910 35

Humans and mice lacking the interferon signaling molecule Stat1 are sensitive to a variety of pathogens due to their presumed inability to mount a strong innate immune response. The herpes simplex virus type 1 (HSV-1) virion host shutoff (vhs) protein is a multifunctional immunomodulator that counteracts the innate immune response and viruses lacking vhs are attenuated and effective live vaccines in animal models. To investigate the interplay of viruses with an immunocompromised host, we performed functional genomics analyses on control and Stat1(-/-) mouse corneas infected with wild-type or vhs-null viruses. In control mice, correlative with viral growth, both viruses induced a transient increase in immunomodulators, followed by viral clearance. In contrast, infection of the Stat1(-/-) mice induced a heightened and prolonged induction of inflammatory modulators for both viruses, manifesting as a significant immune cell infiltrate and ocular disease. Moreover, while wild-type virus infection of Stat1(-/-) was always lethal, vhs-null infection was rarely lethal. There was a significant increase in Stat3- and interleukin-6 (IL-6)-dependent transcription in Stat1(-/-) mice, implicating the Stat3 and IL-6 pathways in the observed ocular pathology. Further, infected Stat1(-/-) mice showed phosphorylated Stat3 in the corneal epithelium. Our data show a role for vhs in evading innate host responses and a role for Stat1 in limiting virus infection and for facilitating an appropriate nonpathological inflammatory response.
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PMID:Host responses to wild-type and attenuated herpes simplex virus infection in the absence of Stat1. 1910 91

It is well established that mediators of peripheral inflammation are relayed to the brain and elicit sickness behavior via neuroinflammatory agents that target neuronal substrates. In the present study, we used double-stranded RNA (dsRNA), a viral replication intermediate, to mimic the acute phase of viral infection. C57BL/6 mice were injected intraperitoneally with 12 mg/kg of synthetic dsRNA, i.e., polyinosinic-polycytidylic acid (PIC). The treatment induced severe sickness behavior in the animals as revealed by the burrowing test performed 6 hr postinjection. PIC challenge also induced up-regulation of mRNA for several cytokines in the brain as determined by real-time quantitative RT-PCR. In all brain regions, i.e., the forebrain, brainstem, and cerebellum, the gene encoding the CXCL2 chemokine featured the most robust up-regulation over the basal level (saline-injected animals), followed by the genes encoding the CCL2 chemokine, interferon-beta (IFNbeta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFalpha), and interleukin-1beta (IL-1beta). The forebrain featured the highest extent of up-regulation of the Ifnb gene, whereas the other genes attained the highest expression in the cerebellum. Most of the genes featured transient up-regulation, with peaks occurring 3-6 hr after PIC challenge. The TNFalpha, CCL2, CXCL2, IFNbeta, and IL-1beta messages remained profoundly up-regulated even at 24 hr. The expression of genes encoding inducible and neuronal nitric oxide synthase (NOS) in the brain was not affected by the peripheral PIC challenge. However, the endothelial NOS message was initially down-regulated and subsequently up-regulated, indicating stimulation of cerebral vasculature.
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PMID:Peripheral challenge with double-stranded RNA elicits global up-regulation of cytokine gene expression in the brain. 1911 8

We report 3 cases of respiratory syncytial virus infection-associated seizures; their abnormalities of cerebrospinal fluid (increased interleukin-6 and positive for virus by highly sensitive assay) were documented. These data revealed that neurological involvement might be caused by a direct invasion.
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PMID:Cerebrospinal fluid analysis in children with seizures from respiratory syncytial virus infection. 1911 45

Glucocorticoids are widely used in the treatment of different inflammatory diseases. The present study was performed to investigate the effect of dexamethasone (DEX) on acute respiratory distress syndrome (ARDS) induced by the H5N1 viral infection in mice. BALB/c mice, 6-8 weeks old, were divided into three groups with 80 mice in each. The infected group and the DEX-treated infected group were inoculated intranasally with 1 x 10(2) 50% mouse infectious dose of A/Chicken/Hebei/108/2002 (H5N1) viruses, with daily intraperitoneal injections of PBS, or 2.5 mg.kg(-1) DEX at days 3-14 post inoculation, respectively. The control group received noninfectious allantoic fluid and a daily intraperitoneal injection of PBS. In H5N1-infected mice, DEX treatment did not improve the mortality (17 out of 20 versus 16 out of 20 deaths in the DEX-treated infected group versus the infected group), and did not alleviate clinical signs, including weight loss, decreased food intake and inactivity. There was no significant amelioration of the hypoxaemia and ARDS-associated pathological changes in DEX-treated infected mice, as assessed by blood gas analysis and histological score. Furthermore, DEX therapy did not inhibit inflammatory cellular infiltration and cytokine release (interleukin-6 and tumour necrosis factor-alpha) in bronchoalveolar lavage fluid induced by the H5N1 infection. In conclusion, dexamethasone treatment (2.5 mg.kg(-1)) from days 3-14 post inoculation has no beneficial effect on acute respiratory distress syndrome caused by the H5N1 infection in mice.
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PMID:Effect of dexamethasone on acute respiratory distress syndrome induced by the H5N1 virus in mice. 1912 72

To examine the effects of macrolide antibiotics on RS virus infection in airways, human tracheal epithelial cells were pre-treated with bafilomycin A(1) and clarithromycin, and infected with RS virus. Viral titers in supernatant fluids and RNA of RS virus, and concentrations of cytokines in supernatant fluids, including interleukin-6 increased with time after infection. Bafilomycin A(1) and clarithromycin reduced viral titers in supernatant fluids of RS virus, RNA of RS virus, the susceptibility to RS virus infection, and concentrations of cytokines induced by virus infection. N-acetyl-S-geranylgeranyl-L-cysteine, an inhibitor for a small GTP binding protein of RhoA, isoform A of the Ras-homologus (Rho) family, an active form of which is associated with RS virus infection via binding to its fusion protein (F protein), reduced viral titers in supernatant fluids and RNA of RS virus. Bafilomycin A(1) and clarithromycin inhibited RhoA activation induced by lysophosphatidic acid in the cells. Fasudil, an inhibitor of Rho kinase, also reduced viral titers in supernatant fluids and RNA of RS virus. These findings suggest that macrolide antibiotics may inhibit RS virus infection, partly through the reduced expression of F protein receptor, activated RhoA, and the inhibition of subsequent Rho kinase activation in human airway epithelial cells.
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PMID:Macrolide antibiotics inhibit respiratory syncytial virus infection in human airway epithelial cells. 1946 56

Dietary fish oils, rich in (n-3) PUFA, including eicosapentaenoic acid and docosahexaenoic acid, have been shown to have antiinflammatory properties. Although the antiinflammatory properties of fish oil may be beneficial during a chronic inflammatory illness, the same antiinflammatory properties can suppress the inflammatory responses necessary to combat acute viral infection. Given that (n-3) fatty acid-rich fish oil supplementation is on the rise and with the increasing threat of an influenza pandemic, we tested the effect of fish oil feeding for 2 wk on the immune response to influenza virus infection. Male C57BL/6 mice fed either a menhaden fish oil/corn oil diet (4 g fish oil:1 g corn oil, wt:wt at 5 g/100 g diet) or a control corn oil diet were infected with influenza A/PuertoRico/8/34 and analyzed for lung pathology and immune function. Although fish oil-fed mice had lower lung inflammation compared with controls, fish oil feeding also resulted in a 40% higher mortality rate, a 70% higher lung viral load at d 7 post infection, and a prolonged recovery period following infection. Although splenic natural killer (NK) cell activity was suppressed in fish oil-fed mice, lung NK activity was not affected. Additionally, lungs of infected fish oil-fed mice had significantly fewer CD8+ T cells and decreased mRNA expression of macrophage inflammatory protein-1-alpha, tumor necrosis factor-alpha, and interleukin-6. These results suggest that the antiinflammatory properties of fish oil feeding can alter the immune response to influenza infection, resulting in increased morbidity and mortality.
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PMID:Fish oil-fed mice have impaired resistance to influenza infection. 1954 56

Adipokines are polypeptides secreted in the adipose tissue in a regulated manner. While some of these molecules are expressed only by adipocytes, resident and infiltrating macrophages and components of the vascular stroma markedly contribute to expression of other adipokines. As a result, adipose tissue inflammation is associated with a modification in the pattern of adipokine secretion. Leptin, adiponectin, and resistin are the best-studied molecules in this class, but cytokines such as tumor necrosis factor or interleukin-6 are also secreted at high levels by the adipose tissue. Several other molecules have been recently identified and are actively investigated. Adipokines interfere with hepatic injury associated with fatty infiltration, differentially modulating steatosis, inflammation, and fibrosis. Several studies have investigated plasma levels of adiponectin in patients with nonalcoholic fatty liver disease, to establish correlations with the underlying state of insulin resistance and with the type and severity of hepatic damage. Hepatitis C is another disease where adipokines may represent a link between viral infection, steatosis, and metabolic disturbances. Identification of the mediators secreted by expanded adipose tissue and their pathogenic role is pivotal in consideration of the alarming increase in the prevalence of obesity and of the detrimental role that this condition exerts on the course of liver diseases.
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PMID:Adipokines in liver diseases. 1958 55


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