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)

Side-stream cigarette smoke has become a hotly debated social, political, and scientific health and safety issue for nonsmokers. The harmful influences of side-stream cigarette smoke on human health are its adverse effects on the immune system, especially when already compromised by other agents. Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by human immunodeficiency virus (HIV). To facilitate studies, murine AIDS was induced in C57BL/6 mice by LP-BM5 murine leukemia virus infection, which mimics human AIDS. After 2 weeks of retroviral infection, the mice were exposed to side-stream cigarette smoke for 30 min, 5 days/week for 12 weeks using a side-stream cigarette smoke exposure system. Murine retrovirus infection reduced the in vitro proliferation of T lymphocytes stimulated by concanavalin A, increased the release of pro-inflammatory cytokine interleukin-6 (IL-6) tumor necrosis factor-alpha (TNF-alpha), increased the hepatic lipid peroxidation and decreased the alpha-tocopherol levels in liver, lung and heart. Concomitant side-stream cigarette smoke exposure for 12 weeks further inhibited the proliferation of T cells, increased the release of TNF-alpha, IL-6 cytokines and enhanced the hepatic lipid peroxidation from retrovirus infected mice. The loss of alpha-tocopherol was also further enhanced by side-stream cigarette smoke exposure during retrovirus infection. Our conclusions are that side-stream cigarette smoke induced increasing oxidative stress, reducing nutrient concentrations and suppressing immune function could make mice with murine AIDS more susceptible to opportunistic infections, potentially accelerating murine AIDS progression. Thus, the reduction of side-stream cigarette smoke exposure is an important health issue in AIDS patients to improve the quality and quantity of their lives.
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PMID:Side-stream cigarette smoke accentuates immunomodulation during murine AIDS. 1209 66

A 27-year-old man presented with fever, convulsive seizure, and sudden impairment of consciousness. Magnetic resonance imaging (MRI) abnormalities were found in the bilateral thalami, including the brain stem and white matter. The possibility of a previous influenza A virus infection was considered, and cerebrospinal fluid cells and interleukin-6 were elevated. The MRI findings closely resembled those found in cases of childhood acute necrotizing encephalopathy (ANE). The present case suggests that adult influenza A virus-associated encephalitis/encephalopathy or ANE can occur during winter influenza epidemics.
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PMID:A case of adult influenza A virus-associated encephalitis: magnetic resonance imaging findings. 1211 48

Regulated on activation, normal T cell expressed, and presumably secreted (RANTES) is a member of the CC chemokine family of proteins implicated in a variety of diseases characterized by lung eosinophilia and inflammation, strongly produced by stimulated airway epithelial cells. Because such cytokines as tumor necrosis factor (TNF)-alpha and interferon-gamma (IFN-gamma) have been shown to enhance RANTES induction in airway epithelial cells and RANTES gene expression appears to be differentially regulated depending on the cell type and the stimulus applied, in this study we have elucidated mechanisms that operate to control RANTES induction on exposure to TNF-alpha and/or IFN-gamma. Our results indicate that TNF-alpha and IFN-gamma synergistically induce RANTES protein secretion and mRNA expression. RANTES transcription is activated only after stimulation with TNF-alpha, but not IFN-gamma, which affects RANTES mRNA stabilization. Promoter deletion and mutagenesis experiments indicate that the nuclear factor (NF)-kappaB site is the most important cis-regulatory element controlling TNF-induced RANTES transcription, although NF-interleukin-6 binding site, cAMP responsive element (CRE), and interferon-stimulated responsive element (ISRE) also play a significant role. TNF-alpha stimulation induces nuclear translocation of interferon regulatory factor (IRF)-3, which in viral infection binds the RANTES ISRE and is necessary for activation of RANTES transcription. However, TNF-induced IRF-3 translocation does not result in IRF-3 binding to the RANTES ISRE. Although viral infection can activate an ISRE-driven promoter, TNF cannot, indicating that RANTES gene enhancers are controlled in a stimulus-specific fashion. Identification of molecular mechanisms involved in RANTES gene expression is fundamental for developing strategies to modulate lung inflammatory responses.
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PMID:Regulation of RANTES promoter activation in alveolar epithelial cells after cytokine stimulation. 1238 74

Dengue virus (DV) replication, antibody-enhanced viral infection, and cytokine responses of human primary B lymphocytes (cells) were characterized and compared with those of monocytes. The presence of a replication template (negative-strand RNA intermediate), viral antigens including core and nonstructural proteins, and increasing amounts of virus with time postinfection indicated that DV actively replicated in B cells. Virus infection also induced B cells to produce interleukin-6 and tumor necrosis factor alpha, which have been previously implicated in virus pathogenesis. In addition, a heterologous antibody was able to enhance both virus and cytokine production in B cells. Furthermore, the levels of virus replication, antibody-enhanced virus replication, and cytokine responses observed in B cells were not statistically different from those in monocytes. These results suggest that B cells may play an important role in DV pathogenesis.
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PMID:Virus replication and cytokine production in dengue virus-infected human B lymphocytes. 1241 63

OBJECTIVE: To investigate the clinical significance of detecting interleukin-6 (IL-6) and interleukin-12 (IL-12) in the immunological mechanism of hepatitis B virus infection (HBV). METHODS: Serum IL-6 and IL-12 levels were determined using enzyme-linked immunosorbent assay in patients with chronic, acute or advanced hepatitis B as well as in healthy subjects. RESULTS: In chronic, acute, severe hepatitis B patients, serum IL-6 levels were significantly elevated as hepatitis worsened (199.7+/-26.9, 129.5+/-22.8, 286.1+/-56.7 pg/ml respectively), in that order compared with the normal control levels (56.41+/-12.9 pg/ml). IL-12 levels, in contrast, tended to be lowered with the deterioration of hepatitis (24.6+/-13.4, 135.3+/-60.8, 19.7+/-9.0 pg/ml respectively), in that order, with the control level of 34.7+/-11.8 pg/ml. CONCLUSION: Serum IL-6 level is closely correlated to the degree of hepatocyte damage in hepatitis B, while IL-12 may be instrumental in the defense mechanism against HBV infection, and IL-12 level elevation can be indicative of hepatitis recovery.
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PMID:Detection of interleukin-6 and -12 in of hepatitis B patients and its clinical significance. 1242 93

Lymphoma cells infected with Kaposi's sarcoma-associated herpesvirus are autocrine dependent on virus-derived interleukin-6 (IL-6), but not on cellular IL-6. During viral infection, host cells induce the antiviral factor interferon (IFN) to up-regulate p21, initiate cell cycle arrest, and inhibit virus replication. Viral IL-6, however, blocks IFN signaling. A viral transcriptional program exists in which only the viral IL-6 gene is directly activated by IFN-alpha, allowing the virus to modify its cellular environment by sensing and responding to levels of intracellular IFN signaling. The human cytokine cannot mimic this effect because IFN-alpha down-regulates the IL-6 receptor, gp80. Viral IL-6 bypasses the gp80 regulatory checkpoint by binding directly to the gp130 transducer molecule, resulting in tumor cell autocrine dependence on the viral cytokine for proliferation and survival.
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PMID:Viral IL-6-induced cell proliferation and immune evasion of interferon activity. 1243 62

Lymphocytic choriomeningitis virus (LCMV) and Lassa virus can cause hemorrhagic fever and liver disease in primates. The WE strain of LCMV (LCMV-WE) causes a fatal Lassa fever-like disease in rhesus macaques and provides a model for arenavirus pathogenesis in humans. LCMV-WE delivered intravenously or intragastrically to rhesus macaques targets hepatocytes and induces high levels of liver enzymes, interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), and soluble tumor necrosis factor receptors (sTNFRI and -II) in plasma during acute infection. Proinflammatory cytokines TNF-alpha and IL-1beta were not detected in plasma of infected animals, but increased plasma gamma interferon was noted in fatally infected animals. Immunohistochemistry of acute liver biopsies revealed that 25 to 40% of nuclei were positive for proliferation antigen Ki-67. The increases in IL-6, sIL-6R, sTNFR, and proliferation antigen that we observe are similar to the profile of incipient liver regeneration after surgical or toxic injury (N. Fausto, Am. J. Physiol. 277:G917-G921, 1999). Although IL-6 was not directly induced by virus infection in vitro, peripheral blood mononuclear cells from acutely infected monkeys produced higher levels of IL-6 upon lipopolysaccharide stimulation than did healthy controls. Our data confirm that acute infection is associated with weak inflammatory responses in tissues and initiates a program of liver regeneration in primates.
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PMID:Arenavirus-mediated liver pathology: acute lymphocytic choriomeningitis virus infection of rhesus macaques is characterized by high-level interleukin-6 expression and hepatocyte proliferation. 1252 6

Measles virus, a paramyxovirus of the Morbillivirus genus, is responsible for an acute childhood illness that infects over 40 million people and leads to the deaths of more than 1 million people annually (C. J. Murray and A. D. Lopez, Lancet 349:1269-1276, 1997). Measles virus infection is characterized by virus-induced immune suppression that creates susceptibility to opportunistic infections. Here we demonstrate that measles virus can inhibit cytokine responses by direct interference with host STAT protein-dependent signaling systems. Expression of the measles V protein prevents alpha, beta, and gamma interferon-induced transcriptional responses. Furthermore, it can interfere with signaling by interleukin-6 and the non-receptor tyrosine kinase, v-Src. Affinity purification demonstrates that the measles V protein associates with cellular STAT1, STAT2, STAT3, and IRF9, as well as several unidentified partners. Mechanistic studies indicate that while the measles V protein does not interfere with STAT1 or STAT2 tyrosine phosphorylation, it causes a defect in IFN-induced STAT nuclear accumulation. The defective STAT nuclear redistribution is also observed in measles virus-infected cells, where some of the STAT protein is detected in cytoplasmic bodies that contain viral nucleocapsid protein and nucleic acids. Interference with STAT-inducible transcription may provide a novel intracellular mechanism for measles virus-induced cytokine inhibition that links innate immune evasion to adaptive immune suppression.
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PMID:STAT protein interference and suppression of cytokine signal transduction by measles virus V protein. 1280 63

Real-time PCR and enzyme-linked immunosorbent assay were used to evaluate the ability of influenza A virus and Streptococcus pneumoniae opacity variants, either alone or in combination, to induce cytokine and chemokine genes in primary cultures of human middle ear epithelial (HMEE) cells. Following treatment with influenza A virus, the induction of gene expression, which occurred in a dose- and time-dependent manner, was strong for macrophage inflammatory protein 1 alpha (MIP-1 alpha) and MIP-1 beta; moderate for tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and IL-8; and weak for IL-1 beta and monocyte chemotactic peptide 1 (MCP-1). Except for TNF-alpha, all the gene products were detected in the cell culture supernatants. In contrast, infection of HMEE cells with S. pneumoniae alone induced low levels of mRNA expression of MIP-1 alpha and MIP-1 beta and did not significantly induce the transcription of the other cytokines and chemokines examined. However, both S. pneumoniae opacity variants increased mRNA expression of MIP-1 alpha, MIP-1 beta, IL-6, and MCP-1 in HMEE cells activated by a prior influenza A virus infection compared to levels in cells treated with either agent alone. Up-regulation of IL-6, IL-8, and MCP-1 mRNA expression and production by the virus in combination with opaque S. pneumoniae was two- to threefold higher than that induced by the virus combined with the transparent S. pneumoniae variant. These data indicate that the activation of HMEE cells by influenza A virus enhances the induction of cytokine and chemokine gene transcripts by S. pneumoniae and that this effect appears to be most pronounced when S. pneumoniae is in the opaque phase.
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PMID:Expression of cytokine and chemokine genes by human middle ear epithelial cells induced by influenza A virus and Streptococcus pneumoniae opacity variants. 1287 4

Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) regulate cardiac hypertrophy. We investigated ventricular alterations of ANP and BNP in interleukin-6 (IL-6) transgenic mice (TG) and wild type (WT) mice with or without viral infection. The ANP and BNP mRNA/GAPDH mRNA ratios in the ventricles of IL-6 TG mice were twice that of WT mice, but were not increased significantly by viral inoculation. In WT mice, both ANP and BNP responses were significantly increased in the ventricles of mice 10 days after encephalomyocarditis (EMC) viral inoculation. Cardiac weight in IL-6 TG mice was significantly greater than in WT 10 days after viral inoculation. Left ventricular wall thickness and the diameter of ventricular myocytes also were greater in IL-6 TG than WT after viral infection. Primary cultures of neonatal rat cardiac myocyte showed that IL-6 increased ANP and BNP mRNA expression in a dose-responsive fashion. In summary, overexpression of ANP and BNP occurs in the ventricles of IL-6 TG mice, along with increased cardiac weight after infection with EMC virus, and impaired responses in the expression of ANP and BNP.
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PMID:Increased cardiac weight in interleukin-6 transgenic mice with viral infection accompanies impaired expression of natriuretic peptide genes. 1288 19


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