UNIPROT:P05231 - FACTA Search

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)

In a preliminary study the hypothesis was tested that cytokine profiles in peripheral blood were higher in women with deep infiltrating endometriosis and cytokine profiles in peritoneal fluid were higher in women with superficial endometriosis. Thirteen women of reproductive age having laparoscopy for infertility (n=9), pain (n=3) or combined pain and infertility (n=1). Peripheral blood and peritoneal fluid were obtained and analyzed for Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-alpha), Interleukin-10 (IL-10), Transforming Growth Factor-betal (TGFbeta1), and Interferon-gamma (IFN-gamma). No significant cytokine differences were observed in either peritoneal fluid or peripheral blood between IL-6, TGFbeta1, IFNgamma, TNF-alpha and IL-10 of women with superficial endometriosis (n=7) and women with deeply infiltrating endometriosis (n=6). The results of this preliminary study do not show significant differences in peripheral blood and peritoneal fluid cytokine levels between women with deep infiltrating endometriosis compared to women with superficial disease. Future studies with increased sample size are required to either confirm or refute these preliminary findings.
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PMID:Cytokine profiles in autologous peritoneal fluid and peripheral blood of women with deep and superficial endometriosis. 1132 93

Interleukin-10 is an important anti-inflammatory and immunosuppressive cytokine with major impact on several immune reactions, including regulatory mechanisms in the skin. Recently, we performed a phase II trial in psoriatic patients receiving subcutaneously interleukin-10 over 7 wk. The clinical response suggested that interleukin-10 might represent a novel anti-psoriatic drug. In order to understand better the mode of action and to elucidate the effects of systemic interleukin-10 treatment on the skin immune system, skin punch biopsies from sites different from interleukin-10 injection were analyzed. Biopsies were obtained from the patients before, at the end, and 3 wk after interleukin-10 therapy. The results are reported here. Histologic examination showed a decrease of several parameters reflecting the psoriatic disease activity as acanthosis and extension of the horny layer. Immunohistologic examination demonstrated decreasing numbers of infiltrating T cells, dermal CD1a+ cells, and a diminished proliferation of epidermal cells. Using a novel, quantitative reverse transcriptase-polymerase chain reaction approach a significant shift within the cytokine pattern was found. Interleukin-10 therapy led to a decrease of cutaneous interleukin-8 and interleukin-10 mRNA expression. Whereas no significant changes of interleukin-6, tumor necrosis factor-alpha, and interferon-gamma expression were found, interleukin-4 was strongly upregulated suggesting a shift from a type 1 towards a type 2 cytokine pattern. The changes within the local cytokine pattern seem to be disease-related, as an inverse course was found in a single interleukin-10 nonresponding patient. Our findings demonstrate considerable effects of systemic interleukin-10 application on the skin immune systems, which might contribute to the anti-psoriatic activity of interleukin-10.
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PMID:Effects of systemic interleukin-10 therapy on psoriatic skin lesions: histologic, immunohistologic, and molecular biology findings. 1134 60

Periprosthetic membranes commonly observed at sites of total joint implant loosening exhibit abundant macrophages and particulate debris. Macrophages phagocytose orthopedic debris and release the pro-inflammatory mediators interleukin-1, interleukin-6, tumor necrosis factor-alpha, and prostaglandin E2. Populations of activated lymphocytes are often seen in periprosthetic membranes. These lymphocytes may modulate the monocyte/macrophage response to particulate debris and influence aseptic loosening. In addition, other immunologic agents, such as interleukin-10, are present in tissues harvested from the bone-implant interface of failed total joint arthroplasties. The present study examined the effects of interleukin-10 on polymethylmethacrylate (PMMA) particle challenged human monocyte/macrophages in vitro. Human monocyte/macrophages isolated from buffy coats of five healthy individuals were exposed to 1-10 microm PMMA particles. Interleukin-10 was added to the monocyte/macrophages with and without the addition of PMMA particles. Interleukin-10-induced alterations in monocyte/macrophage metabolism were determined measuring interleukin-6 and tumor necrosis factor-alpha release by the cells following exposure to PMMA particles. Exposure of the monocyte/macrophages to PMMA particles resulted in a dose-dependent release of interleukin-6 and tumor necrosis factor-alpha at 48 h. Interleukin-10 reduced the levels of interleukin-6 and tumor necrosis factor-alpha release by macrophages in response to PMMA particles in a dose-dependent manner. At 48 h, particle-induced interleukin-6 release was inhibited by 60 and 90% with 1.0 and 10.0 ng/ml treatments of interleukin-10, respectively. At 48 h, particle-induced tumor necrosis factor-alpha release was inhibited by 58 and 88% with 1.0 and 10.0 ng/ml treatments of interleukin-10, respectively. Interleukin-10 challenge alone did not significantly alter basal interleukin-6 or tumor necrosis factor-alpha release relative to control cultures. The data presented in this study demonstrate that the anti-inflammatory cytokine, interleukin-10, inhibits monocyte/macrophage release of the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha in response to PMMA particle challenge in vitro.
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PMID:Interleukin-10 inhibits polymethylmethacrylate particle induced interleukin-6 and tumor necrosis factor-alpha release by human monocyte/macrophages in vitro. 1143 85

Interleukin-10 (IL-10) exerts a wide spectrum of regulatory activities in the immune and inflammatory response. The aim of this study was to investigate the role of endogenous IL-10 in the modulation of the inflammatory response in mice subjected to collagen-induced arthritis. Collagen-induced arthritis (CIA) was induced in mice lacking the gene for IL-10 (IL-10 "knock-out", IL-10KO) and in wild-type control (IL-10WT) mice by an intradermal injection of 100 mul of the emulsion (containing 100 mug of bovine type II collagen) (CII) and complete Freund's adjuvant (CFA) at the base of the tail. On day 21, a second injection of CII in CFA was administered. IL-10 wild type (WT) mice developed an erosive, hind paw arthritis when immunised with CII in CFA. Macroscopic clinical evidence of CIA first appeared as peri-articular erythema and oedema in the hind paws. The incidence of CIA was 100% by day 27 in the CII-challenged IL-10WT. The severity of CIA progressed over a 35-day period, with radiographic evaluation revealing focal resorption of bone. The histopathology of CIA included erosion of the cartilage at the joint margins. IL-10KO mice experienced higher rates of clinical signs and more severe knee and paw injury as compared to IL-10WT. The degree of oxidative and nitrosative damage was significantly higher in IL-10KO mice than in wild-type littermates, as indicated by elevated malondialdehyde levels and formation of nitrotyrosine and poly (ADP-ribose) synthetase (PARS). Plasma levels of the proinflammatory cytokines, tumour necrosis factor, interleukin-1beta and interleukin-6 were also greatly enhanced in comparison to wild-type mice. These data demonstrate that endogenous IL-10 exerts an anti-inflammatory role during chronic inflammation and tissue damage associated with collagen-induced arthritis, possibly by regulating neutrophil recruitment, and the subsequent cytokine and oxidant generation.
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PMID:Absence of endogeneous interleukin-10 enhances the evolution of murine type-II collagen-induced arthritis. 1178 Nov 83

Interleukin-10 (IL-10) exerts a wide spectrum of regulatory activities in the immune and inflammatory response. The aim of this study was to investigate the role of endogenous IL-10 on the modulation of the inflammatory response in mice subjected to carrageenan-induced lung injury. When compared to carrageenan-treated IL-10 wild-type (WT) mice, carrageenan-treated IL-10 knock-out mice (IL-10KO) mice experienced a higher rate of pleural exudation, and polymorphonuclear cell migration. Exudate levels of the pro-inflammatory cytokines tumour necrosis factor, interleukin-1beta and interleukin-6 were also greatly enhanced in IL-10KO mice in comparison to wild-type mice. Lung myeloperoxidase (MPO) activity was significantly reduced in IL-10WT mice when compared to IL-10KO mice-treated with carrageenan. The degree of oxidative and nitrosative damage was significantly higher in IL-10KO mice than in wild-type littermates, as indicated by elevated malondialdehyde levels and formation of nitrotyrosine and poly (ADP-ribose) synthetase (PARS). Staining of lung tissue sections obtained from carrageenan-treated IL-10WT with an anti-COX-2 antibody showed a positive staining of the inflamed tissue. Furthermore, expression of inducible nitric oxide synthase (iNOS) was found mainly in the macrophages of the inflamed lungs from carrageenan-treated IL-10WT mice. The intensity and degree of the staining for COX-2 and iNOS were markedly enhanced in tissue sections obtained from carrageenan-treated IL-10KO mice. Most notably, the degree of lung injury caused by carrageenan was also enhanced in IL-10KO mice. Taken together, our results clearly demonstrate that endogenous IL-10 exerts an anti-inflammatory role during acute inflammation and tissue damage associated with carrageenan-induced pleurisy, possibly by regulating neutrophil recruitment, and the subsequent cytokine and oxidant generation.
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PMID:Absence of endogenous interleukin-10 enhances the evolution of acute lung injury. 1223 72

Local and systemic temperature change is associated with the immune response to infection, but the role of temperature remains poorly understood. To study the effect of temperature on macrophage activation by lipopolysaccharide (LPS), RAW 264.7 cells were incubated with LPS at different temperatures and secretion of three cytokines was measured. Incubation at 31 degrees C increased tumour necrosis factor (TNF) secretion when compared with 37 degrees C, while cells exposed at 39 degrees C secreted less TNF. Interleukin-6 (IL-6) secretion was less at 31 degrees C than at 37 degrees C and remained unchanged at 39 degrees C. Interleukin-10 secretion was depressed on either side of 37 degrees C. Only IL-6 secretion was sensitive to preincubation temperature effects. The kinetics of cytokine secretion and steady-state mRNA analysis indicated potentially different mechanisms of temperature regulation for TNF and IL-6.
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PMID:Temperature alters lipopolysaccharide-induced cytokine secretion by RAW 264.7 cells. 1282 58

The designation of atherosclerosis as a chronic inflammatory process represents an interesting paradigmatic shift for cardiologists. The plasma concentrations of interleukin-6 and its hepatic byproduct, C-reactive protein, may reflect the intensity of occult plaque inflammation and the vulnerability to rupture. Monocyte chemoattractant protein-1 and interleukin-8 play a crucial role in initiating atherosclerosis by recruiting monocytes/macrophages to the vessel wall, which promotes atherosclerotic lesions and plaque vulnerability. In addition, circulating levels of these proinflammatory cytokines increase in patients with acute myocardial infarction and unstable angina, but not in those with stable angina. Also, the plasma concentrations of these cytokines increase after percutaneous coronary intervention, causing late restenosis after the procedure. Angiotensin II and other atherogenic factors induce these cytokines in the cardiovascular tissues through the activation of transcription factors, such as nuclear factor-kappaB or peroxisome proliferator-activated receptors. Conversely, HMG-CoA reductase inhibitors (statins) can potently inhibit these proinflammatory factors in the vessels. A small GTP-binding protein, Rho, may be a key molecule to explain the anti-inflammatory effects of statins. Interleukin-10 also exerts anti-inflammatory effects on the cardiovascular tissues, possibly by deactivating proinflammatory cytokines and inducible nitric oxide synthase. Gene therapy using interleukin-10 may be a promising means for untreatable or complicated cases of cardiovascular diseases. Thus, therapeutic modulations of these inflammatory cytokines may be useful in the prevention of atherosclerosis and future cardiovascular events.
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PMID:Inflammatory cytokines and cardiovascular disease. 1456 Nov 60

The effect of aqueous extract of Swertia chirayita stem on the pro- and anti-inflammatory cytokines balance in primary joint synovium of adjuvant-induced arthritic mice has been studied. The level of pro-inflammatory cytokines was found elevated in the joint synovium of arthritic mice in comparison to normal joints. Administration of S. chirayita extract in varying doses through the oral route did not modulate the proinflammatory cytokines on day 2. In contrast, by day 12, a dose dependent (0, 11.86 and 23.72 mg/kg body weight) reduction of tumor necrosis factor-alpha (INF-alpha) interleukin-1beta, (IL-beta) and interferon-gamma, (IFN-gamma) and elevation of Interleukin-10 (IL-10) was observed in the joint homogenates of arthritic mice. Interleukin-6 (IL-6) was not down regulated in joint homogenate of arthritic mice at the dose 11.86 mg/kg but at higher doses (23.72 and 35.58 mg/kg) significant reduction was observed. The aqueous extract was found to possess two polar compounds, amerogentin and mangiferin but was devoid of swerchirin, chiratol, methyl swetianin, and swertanone. Mangiferin has been reported to possess potent anti-inflammatory property and we presume its presence in the aqueous extract of S. chirayita is responsible for reducing TNF-alpha, IL-1beta, IL-6, and IFN-gamma and/or elevating IL-10 in the joint homogenates of arthritic mice on day 12. This study will help in our understanding of the mechanism of anti-inflammatory action of S. chirayita in the light of proinflammatory and anti-inflammatory cytokine balance.
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PMID:Swertia chirayita mediated modulation of interleukin-1beta, interleukin-6, interleukin-10, interferon-gamma, and tumor necrosis factor-alpha in arthritic mice. 1468 99

Microendoscopic discectomy (MED) has been accepted as a minimally invasive procedure for lumbar discectomy because of the small skin incision and short hospital stay required for this surgery. However, there are few objective laboratory data to confirm the reduced systemic responses in the early phase after this procedure. In order to substantiate the reduced invasiveness of MED compared to microdiscectomy (MD) or procedures involved in one-level unilateral laminotomy, the invasiveness of each surgical procedure was evaluated by measuring serum levels of biochemical parameters reflective of a post-operative inflammatory reaction and damage to the paravertebral muscles. Thirty-three patients who underwent lumbar discectomy or one-level unilateral laminotomy (MED in 15 cases, MD in 11 cases and one-level unilateral laminotomy in 7 cases with lumbar spinal canal stenosis) were included in this study. The serum levels of C-reactive protein (CRP) and creatine phosphokinase (CPK) were measured at 24 h after operation. Interleukin-6 (IL-6) and Interleukin-10 (IL-10) were measured at 2, 4, 8 and -24 h following the surgery to monitor the inflammatory response to the respective surgery. The post-operative serum CRP levels from both the MD and MED groups were significantly lower than those from the open laminotomy group. However, there was no significant difference in these serum levels between the MED and MD groups. The levels of IL-6 and IL-10 in the MED group during the first post-operative day were also significantly lower than those in the laminotomy group. When the MED and MD groups were compared, the IL-6 levels in the MED group were lower than in MD group at 2, 4 and 8 h after surgery, but the differences were not statistically significant. However, the level was significantly lower in the MED group at 24 h after surgery. In terms of IL-10, no significant difference was noted between the MED and MD groups over the study period. The changes in serum levels of post-operative inflammatory: markers (CRP, IL-6 and IL-10) in the early phase indicated reduced inflammatory reactions in MED as well as in MD when compared with classical open unilateral laminotomy. These data draw a direct link between the lower level of the inflammatory response and reduced invasiveness of MED. However, an indicator for muscle damage (CPK) appeared not to be affected by the type of surgical procedure used to correct disc herniation.
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PMID:Objective assessment of reduced invasiveness in MED. Compared with conventional one-level laminotomy. 1592 58

We measured levels of six cytokines and human immunodeficiency virus (HIV) RNA in saliva from HIV-seropositive individuals and compared salivary cytokine levels in HIV-seropositives and seronegatives. All of the six tested cytokines were detected in saliva although interleukin-1beta, interferon-gamma and interleukin-10 were detected more frequently (90%, 68% and 61% of samples, respectively) than interleukin-6, tumor necrosis factor-alpha and tumor necrosis factor-alpha receptor II (2-17%). There was no significant association between cytokine levels in saliva and plasma suggesting that cytokines were produced locally. Interferon-gamma levels were significantly higher in saliva from HIV-seropositives when compared to seronegatives while interleukin-10 levels were lower in seropositive saliva. Interleukin-10 levels were higher in individuals with low CD4 counts in the seropositive group. HIV RNA was detected in 29% of saliva samples from seropositives and there was a significant correlation between saliva and plasma HIV RNA levels. However, HIV RNA levels in saliva were not significantly associated with any of the saliva or plasma cytokine levels or with CD4 cell numbers. This study shows no association between inflammatory cytokine levels and HIV levels in saliva and suggests that saliva HIV levels are more influenced by blood HIV RNA levels than oral inflammation.
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PMID:Relationship of HIV RNA and cytokines in saliva from HIV-infected individuals. 1605 Oct 64

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