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Cytokines IL-6 (cytokine + il-6)

Distribution by Scientific Domains
Medical Sciences66%
Life Sciences33%

Kinds of Cytokines IL-6

  • proinflammatory cytokine il-6
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    Selected Abstracts

    Distinct roles of protein kinase R and toll-like receptor 3 in the activation of astrocytes by viral stimuli

    GLIA, Issue 3 2007
    Pamela A. Carpentier
    Abstract Impaired immune surveillance and constitutive immunosuppressive properties make the central nervous system (CNS) a particular challenge to immune defense, and require that CNS-resident cells be capable of rapidly recognizing and responding to infection. We have previously shown that astrocytes respond to treatment with a TLR3 ligand, poly I:C, with the upregulation of innate immune functions. In the current study, we examine the activation of innate immune functions of astrocytes by Theiler's murine encephalomyelitis virus (TMEV), a picornavirus, which establishes a persistent infection in the CNS of susceptible strains of mice and leads to the development of an autoimmune demyelinating disease that resembles human multiple sclerosis. Astrocytes infected with TMEV are activated to produce type I interferons, the cytokine IL-6, and chemokines CCL2 and CXCL10. We further examined the mechanisms that are responsible for the activation of astrocytes in response to direct viral infection and treatment with poly I:C. We found that the cytoplasmic dsRNA-activated kinase PKR is important for innate immune responses to TMEV infection, but has no role in their induction by poly I:C delivered extracellularly. In contrast, we found that TLR3 has only a minor role in responses to TMEV infection, but is important for responses to poly I:C. These results highlight the differences between responses induced by direct, nonlytic virus infection and extracellular poly I:C. The activation of astrocytes through these different pathways has implications for the initiation and progression of viral encephalitis and demyelinating diseases such as multiple sclerosis. © 2006 Wiley-Liss, Inc. [source]

    Evidence of active cytomegalovirus infection and increased production of IL-6 in tissue specimens obtained from patients with inflammatory bowel diseases

    INFLAMMATORY BOWEL DISEASES, Issue 3 2003
    Afsar Rahbar
    Abstract Recent reports have focused interest on human cytomegalovirus (HCMV) in inflammatory bowel diseases (IBD). Our aim in this study was to examine the frequency of HCMV-infected intestinal cells in tissue sections obtained from patients with IBD, and to investigate if HCMV-infected intestinal cells produce the proinflammatory cytokine IL-6. We studied intestinal tissue sections from 13 patients with ulcerative colitis, 10 with Crohn's disease, 10 cancer patients without intestinal inflammation, and 10 samples from HCMV-infected AIDS patients. HCMV-DNA was detected by in situ hybridization in sections obtained from 12/13 patients with ulcerative colitis, in 10 with Crohn's disease, in 10/10 samples from HCMV-infected AIDS patients, but not in any of the 10 samples that were obtained from uninflamed tissues. HCMV-specific antigens were detected in samples from all HCMV-infected AIDS patients, in 11/13 sections from patients with ulcerative colitis, in 10/10 samples from patients with Crohn's disease, but not in sections from uninflamed tissues. Cells were double positive for an HCMV early antigen and IL-6 in 10/13 sections from patients with ulcerative colitis, in all patients with Crohn's disease, and in 4/10 samples from AIDS patients. In conclusion, these results suggest that active HCMV infection in the intestine is very frequent in patients with IBD, and may contribute to the inflammatory process through an increased production of IL-6. [source]

    C5a modulation of interleukin-1, -induced interleukin-6 production by human osteoblast-like cells

    JOURNAL OF PERIODONTAL RESEARCH, Issue 3 2000
    John M. Pobanz
    Periodontal bone resorption is controlled by osteoblast products, including interleukin (IL)-6, which are stimulated by other cytokines and complement components in the pro-inflammatory milieu. This study demonstrated that human osteoblast-like osteosarcoma cells (MG-63) responded to human recombinant (hr) C5a by releasing significant amounts of the bone-resorbing cytokine IL-6. C5a-induced release of IL-6 was enhanced 330% when cells were exposed to IL-1, prior to C5a challenge at optimal concentrations (1.0 ,g/ml C5a, 0.1 ng/ml IL-1,). Cells simultaneously challenged with these concentrations of C5a and IL-1, produced a 700% increase in IL-6 release relative to cells challenged with IL-1, alone. Incubation of IL-1,-treated cells with anti-human C5a receptor (C5aR) Ab resulted in a 78% suppression of the C5a-induced release of IL-6, but C5aR neutralization did not affect C5a/IL-1, co-stimulation of IL-6. In addition, neither IL-1, nor C5a significantly altered the other's cell-surface receptor relative to binding affinity or density. These results indicate that while MG-63 cells express functional C5aRs, the synergistic effect of C5a and IL-1, on osteoblast IL-6 production is probably controlled by post-receptor signaling events. C5a agonists and antagonist used to alter critical C5a concentrations may present a new point of therapeutic intervention for the treatment of inflammatory bone resorption such as is found in periodontitis. [source]

    The effect of adrenomedullin and cold stress on interleukin-6 levels in some rat tissues

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2010
    N. C. Yildirim
    Summary Stress known to stimulate sympathetic activity, as well as the hypothalamic,pituitary,adrenal axis (HPA), produces a significant increase in adrenomedullin (AdM) levels, suggesting a regulatory or protective role for AdM in countering HPA activation that follows a variety of stressors. Stressors can modulate the secretion of proinflammatory cytokines. Interleukin (IL)-6 is a potent activator of the HPA and appears to play a pathogenic role in conditions related to stress. In the present study, we investigated the administration of AdM on IL-6 levels in cold exposed rats. Male Wistar rats were divided into four groups as control, adrenomedullin treatment, cold stress and cold stress+adrenomedullin-treated groups. In the adrenomedullin-treated group, animals received intraperitoneal (i.p.) injection of adrenomedullin (2000 ng/kg body weight) once a day for a week. For the cold stress exposure the rats were kept in separate cages at 10°C for a week. Control group rats were kept in laboratory conditions. The concentration of IL-6 was determined using an enzyme-linked immunosorbent assay (ELISA) kit. When compared to control, IL-6 levels increased significantly in the cold stress- and adrenomedullin-treated groups (P < 0·05). Administration of AdM in addition to cold stress decreased IL-6 levels in lung and liver, but increased in brain and heart when compared to control (P < 0·05). The results suggest that cold stress may induce increase of rat proinflammatory cytokine IL-6 and adrenomedullin may play a regulatory or protective role for cold stress. [source]

    Effect of pro-inflammatory and immunoregulatory cytokines on human tenocytes

    JOURNAL OF ORTHOPAEDIC RESEARCH, Issue 8 2010
    Thilo John
    Abstract Tendon injury induces a local inflammatory response, characterized by the induction of pro-inflammatory cytokines. The aim of the present study was to analyze the effects of TNF,, IL-6 and IL-10 on key parameters of tendon homeostasis. Cultured primary human tenocytes were treated with the recombinant cytokines IL-6, IL-10, TNF,, or combinations of TNF, with IL-6 and IL-10 (10 ng/mL, 6, 24 h). Expression of type I collagen, elastin, MMP-1, TNF,, IL-1,, IL-6, IL-10, and suppressors of cytokine signaling (SOCS1, 3) was analyzed with the use of RTD-PCR, immunocytochemistry, and Western blot analysis. In response to TNF,, tenocytes reduced their type I collagen deposition but increased their elastin gene expression and highly upregulated their expression for MMP-1, pro-inflammatory (TNF,, IL-1,) and immunoregulatory (IL-6, IL-10) cytokines. TNF, stimulation augmented SOCS1, whereas SOCS3 expression in tenocytes was also induced by IL-6. The treatment of tenocytes with IL-6 and IL-10 had no effect on cytokine expression. Neither IL-6 nor IL-10 modulated the observed effects of TNF, significantly. These results indicate that TNF, strongly activates the tenocytes to amplify their own TNF, expression and, subsequently, that of other regulatory cytokines and matrix degrading enzymes. However, the impact of IL-6 and IL-10 on tenocytes remains unclear. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:1071,1077, 2010 [source]

    Effects of Bifidobacterium bifidum on adaptive immune senescence in aging mice

    MICROBIOLOGY AND IMMUNOLOGY, Issue 10 2010
    Yu-Rong Fu
    ABSTRACT Bifidobacteria are a natural component of the bacterial flora of the human body and have a symbiotic bacteria-host relationship with human beings. Aging is associated with reduced numbers of beneficial colonic Bifidobacteria and impaired immunity. The possible anti-senescence effects of Bifidobacteria are presently unknown. The aims of the present study were to investigate possible anti-senescence effects of B. bifidum on naturally senescent mice and to explore their mechanisms. After treatment with B. bifidum, mice were killed and samples collected. Cytokine production in serum and lymphocyte culture supernatant, anti-oxidation activity and gene expression were measured. B. bifidum significantly increased cytokine IL-2 and IFN-, levels but decreased proinflammatory cytokines IL-6 and TNF-, concentrations. Moreover, B. bifidum improved anti-oxidation activity and reduced lipid peroxidation in thymus and spleen. In addition, B. bifidum down-regulated p16 expression in thymus and spleen. Taken together, the results indicate, for the first time, that B. bifidum delays senescence by several mechanisms, including enhancement of anti-oxidation activity in thymus and spleen, alteration of gene expression and improvement in immune function. [source]

    Antimicrobial and anti-inflammatory activity of five Taxandria fragrans oils in vitro

    MICROBIOLOGY AND IMMUNOLOGY, Issue 11 2008
    Katherine A. Hammer
    ABSTRACT The antimicrobial activity of five samples of Taxandria fragrans essential oil was evaluated against a range of Gram-positive (n= 26) and Gram-negative bacteria (n= 39) and yeasts (n= 10). The majority of organisms were inhibited and/or killed at concentrations ranging from 0.06,4.0% v/v. Geometric means of MIC were lowest for oil Z (0.77% v/v), followed by oils X (0.86%), C (1.12%), A (1.23%) and B (1.24%). Despite differences in susceptibility data between oils, oils A and X did not differ when tested at 2% v/v in a time kill assay against Staphylococcus aureus. Cytotoxicity assays using peripheral blood mononuclear cells demonstrated that T. fragrans oil was cytotoxic at 0.004% v/v but not at 0.002%. Exposure to one or more of the oils at concentrations of ,0.002% v/v resulted in a dose responsive reduction in the production of proinflammatory cytokines IL-6 and TNF-,, regulatory cytokine IL-10, Th1 cytokine IFN-, and Th2 cytokines IL-5 and IL-13 by PHA stimulated mononuclear cells. Oil B inhibited the production of all cytokines except IL-10, oil X inhibited TNF-,, IL-6 and IL-10, oil A inhibited TNF-, and IL-6, oil C inhibited IL-5 and IL-6 and oil Z inhibited IL-13 only. IL-6 production was significantly inhibited by the most oils (A, B, C and X), followed by TNF-, (oils A, B and X). In conclusion, T. fragrans oil showed both antimicrobial and anti-inflammatory activity in vitro, however, the clinical relevance of this remains to be determined. [source]

    The host cytokine response to Porphyromonas gingivalis is modified by gingipains

    MOLECULAR ORAL MICROBIOLOGY, Issue 1 2009
    P. G. Stathopoulou
    Background/aims:, Clinical studies indicate that primary proinflammatory cytokines, such as interleukin-1, (IL-1,) are elevated in the gingival crevice around teeth with periodontitis but the secondary cytokines and chemokines, IL-6 and IL-8, are not. The human gingival epithelial cells (HGECs) lining the gingival sulcus respond to perturbation by microbes of dental plaque by releasing a wide range of cytokines. Porphyromonas gingivalis, a putative periodontal pathogen, possesses numerous virulence factors some of which directly impact on the host response. In the present study, we sought to determine how P. gingivalis influences the inflammatory cytokine responses. Methods:, HGECs were challenged with P. gingivalis and other putative periodontal pathogens, and the resultant production of IL-1,, IL-6, and IL-8 was assayed by enzyme-linked immunosorbent assay (ELISA). Culture supernatants and recombinant human cytokines were challenged with live P. gingivalis wild-type and gingipain-deficient strains and the resultant cytokine profile was assessed by ELISA and Western blot. Results:, We show here that primary HGECs challenged with live P. gingivalis result in high levels of IL-1, but not the related secondary cytokines IL-6 and IL-8. We further demonstrate that cytokine response differences are the result of the action of P. gingivalis proteases, with lysine gingipain being the most effective. Conclusion:, We conclude that P. gingivalis, through lysine gingipain, can subvert the protective host proinflammatory response by direct cytokine degradation. Changes in the crevicular cytokine profile have consequences in periodontal disease pathogenesis that should be considered in the development of diagnostic and therapeutic modalities. [source]

    Brain Death Activates Donor Organs and Is Associated with a Worse I/R Injury After Liver Transplantation

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 6 2007
    S. Weiss
    The majority of transplants are derived from donors who suffered from brain injury. There is evidence that brain death causes inflammatory changes in the donor. To define the impact of brain death, we evaluated the gene expression of cytokines in human brain dead and ideal living donors and compared these data to organ function following transplantation. Hepatic tissues from brain dead (n = 32) and living donors (n = 26) were collected at the time of donor laparotomy. Additional biopsies were performed before organ preservation, at the time of transplantation and one hour after reperfusion. Cytokines were assessed by real-time reverse transcriptase,polymerase chain reaction (RT,PCR) and cytometric bead array. Additionally, immunohistological analysis of tissue specimens was performed. Inflammatory cytokines including IL-6, IL-10, TNF-,, TGF-, and MIP-1, were significantly higher in brain dead donors immediately after laparotomy compared to living donors. Cellular infiltrates significantly increased in parallel to the soluble cytokines IL-6 and IL-10. Enhanced immune activation in brain dead donors was reflected by a deteriorated I/R injury proven by elevated alanin-amino-transferase (ALT), aspartat-amino-transferase (AST) and bilirubin levels, increased rates of acute rejection and primary nonfunction. Based on our clinical data, we demonstrate that brain death and the events that precede it are associated with a significant upregulation of inflammatory cytokines and lead to a worse ischemia/reperfusion injury after transplantation. [source]

    A role for ,/, T cells in a mouse model of fracture healing

    ARTHRITIS & RHEUMATISM, Issue 6 2009
    Nona T. Colburn
    Objective Fractures can initiate an immune response that disturbs osteoblastic and osteoclastic cellular homeostasis through cytokine production and release. The aim of our study was to investigate ,/, T cells, innate lymphocytes known to be involved in tissue repair, as potential cellular components of the osteoimmune system's response to an in vivo model of bone injury. The absence of such cells or their effector cytokines influences the fate of other responder cells in proliferation, differentiation, matrix production, and ultimate callus formation. Methods Tibia fractures were created in 60 ,/, T cell,deficient mice (also called , T cell receptor [TCR],knockout mice) and 60 control C57BL/6 mice. Analysis included radiographs, basic histology, mechanical testing, flow cytometry, and immunohistochemical localization of ,/, TCR,positive subsets from control animals and of CD44 expression from both groups, as well as enzyme-linked immunosorbent assay for the effector cytokines interleukin-2 (IL-2), interferon-, (IFN,), and IL-6. Results Animals deficient in ,/, T cells demonstrated more mature histologic elements and quantitative increases in the expression of major bone (bone sialoprotein) and cartilage (type II collagen) matrix proteins and in the expression of bone morphogenetic protein 2 at a critical reparative phase. Moreover, only ,/, T cell,deficient animals had a decrease in the osteoprogenitor antiproliferative cytokines IL-6 and IFN, at the reparative phase. The result was improved stability at the repair site and an overall superior biomechanical strength in ,/, T cell,deficient mice compared with controls. Conclusion The evidence for a role of ,/, T cells in the context of skeletal injury demonstrates the importance of the immune system's effect on bone biology, which is relevant to the field of osteoimmunology, and offers a potential molecular platform from which to develop essential therapeutic strategies. [source]

    Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis

    ARTHRITIS & RHEUMATISM, Issue 4 2009
    Francesco Ciccia
    Objective Subclinical gut inflammation is common in spondylarthritis, but the immunologic abnormalities underlying this process are undefined. Perturbation of the interleukin-23 (IL-23)/Th17 axis has emerged as a fundamental trigger of chronic inflammation. This study was undertaken to investigate the expression and tissue distribution of IL-23/Th17,related molecules in Crohn's disease (CD) and in subclinical gut inflammation in ankylosing spondylitis (AS). Methods Quantitative gene expression analysis of Th1/Th2 and IL-23/Th17 responses was performed in intestinal biopsy samples obtained from 12 patients with CD, 15 patients with AS, and 13 controls. IL-23 tissue distribution and identification of IL-23,producing cells were evaluated by immunohistochemistry. Results We demonstrated a strong and significant up-regulation of IL-23p19 transcripts in the terminal ileum in patients with AS and patients with CD. IL-23 was abundantly produced by infiltrating monocyte-like cells in inflamed mucosa from AS and CD patients. Notably, we also identified Paneth cells as a major source of IL-23 in patients with AS, patients with CD, and normal controls. Unlike CD, in AS patients, IL-23 was not associated with up-regulation of IL-17 and the IL-17,inducing cytokines IL-6 and IL-1,. Finally, while the Th1-related cytokines interferon-,, IL-12p35, and IL-27p28 were overexpressed only in CD patients, IL-4, IL-5, and STAT-6 were also significantly increased in AS patients. Conclusion Our findings indicate that overexpression of IL-23, but not IL-17, is a pivotal feature of subclinical gut inflammation in AS. Identification of resident Paneth cells as a pivotal source of IL-23 in physiologic and pathologic conditions strongly suggests that IL-23 is a master regulator of gut mucosal immunity, providing a pathophysiologic significance to the reported association between IL-23 receptor polymorphisms and intestinal inflammation. [source]

    Proinflammatory cytokines (IL-17, IL-6, IL-18 and IL-12) and Th cytokines (IFN- ,, IL-4, IL-10 and IL-13) in patients with allergic asthma

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 2 2001
    C. K. Wong
    Allergen-reactive T helper type-2 (Th2) cells and proinflammatory cytokines have been suggested to play an important role in the induction and maintenance of the inflammatory cascade in allergic asthma. We compared the plasma concentrations of novel proinflammatory cytokines IL-17 and IL-18, other proinflammatory cytokines IL-6 and IL-12, Th2 cytokines IL-10 and IL-13, and intracellular interferon- , (IFN- ,) and IL-4 in Th cells of 41 allergic asthmatics and 30 sex- and age-matched health control subjects. Plasma cytokines were measured by enzyme-linked immunosorbent assay. Intracellular cytokines were quantified by flow cytometry. Plasma IL-18, IL-12, IL-10, IL-13 concentrations were significantly higher in allergic asthmatic patients than normal control subjects (IL-18: median 228·35 versus 138·72 pg/ml, P < 0·001; IL-12: 0·00 versus 0·00 pg/ml, P = 0·001; IL-10: 2·51 versus 0·05 pg/ml, P < 0·034; IL-13: 119·38 versus 17·89 pg/ml, P < 0·001). Allergic asthmatic patients showed higher plasma IL-17 and IL-6 concentrations than normal controls (22·40 versus 11·86 pg/ml and 3·42 versus 0·61 pg/ml, respectively), although the differences were not statistically significant (P = 0·077 and 0·053, respectively). The percentage of IFN- , -producing Th cells was significantly higher in normal control subjects than asthmatic patients (23·46 versus 5·72%, P < 0·001) but the percentage of IL-4 producing Th cells did not differ (0·72 versus 0·79%, P > 0·05). Consequently, the Th1/Th2 cell ratio was significantly higher in normal subjects than asthmatic patients (29·6 versus 8·38%, P < 0·001). We propose that allergic asthma is characterized by an elevation of both proinflammatory and Th2 cytokines. The significantly lower ratio of Th1/Th2 cells confirms a predominance of Th2 cells response in allergic asthma. [source]