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 interactions between Chlamydia trachomatis and human blood mononuclear leukocytes were studied using flow cytometry, immunofluorescence, electron microscopy and cytokine assays. Under serum-free conditions, elementary bodies (EB) of C. trachomatis were found to bind to human T lymphocytes as well as to B cells and monocytes/macrophages (M phi). For all cell types the binding was saturable, rapid, temperature-independent and independent of the chlamydia-specific serological status of the donor. Similar proportions of T and B cells bound EB at similar levels. In the T cell population, proportionally less CD8+ cells bound EB. Whereas M phi phagocytosed and destroyed the bound micro-organisms for lymphocytes, the Chlamydia remained at the surface, adherent to morphologically featureless membrane areas and showed no evidence of uptake even after long periods at 37 degrees C. Host molecules modulated these basic binding patterns: a heat-stable serum factor inhibited EB binding to T cells and a heat-labile serum factor enhanced binding to B cells. Stimulation with C. trachomatis EB rapidly elicited cytokine production by lymphocytes including interleukin-6 from B cells and interferon-gamma (IFN-gamma) from T and/or nonT/nonB cells. The responses were irrespective of the serological status of the donor. The findings suggest that C. trachomatis-leucocyte interactions may differ from the interactions of other bacteria and human leucocytes. The possible relationship between leucocyte-binding, cytokine induction, and the pathognomonic development of lymphoid follicles during mucosal C. trachomatis infections is discussed.
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PMID:Preferential binding of Chlamydia trachomatis to subsets of human lymphocytes and induction of interleukin-6 and interferon-gamma. 178 4

This review compares the clinical usefulness of immunological methods for the detection of structural components and metabolites of bacteria and fungi. Bacterial antigens (especially those of Mycobacterium, Neisseria, Staphylococcus aureus, Yersinia enterocolitica, Escherichia coli, Salmonella, Chlamydia, and Brucella) are best detected by enzyme-linked immunosorbent assay. Methods involving antibodies are more expensive and are effective only when performed in series. The detection of antibodies that recognize S aureus teichoic acid merely confirms the presence of a metastatic complication. Tissue invasion by Candida albicans is not yet reliably detectable by the presence of a specific antigen. Simple, but not completely reliable methods are available such as the latex test for mannans detection and/or agglutination with liposomes for detecting 48-kDa cytoplasmic protein antigen and an assay for detecting enolase antigen. A latex agglutination test has also been developed for the mannans antigen of Aspergillus and for Cryptococcus neoformans capsular polysaccharide; the latter test is more cost effective. The sensitivity of both tests is improved by serial assays. A negative finding with hemagglutination-based antibody tests rules out C albicans infection, and titers of 1/640 or higher have been associated with disseminated infection by Aspergillus. Concentrations of C albicans blastopore antigen antibodies higher than 400 IU/ml can be seen in disseminated candidiasis. High concentrations of endotoxin are indicative of imminent septic shock. Some biological indicators (C reactive protein, angiotensin converting enzyme, fibronectin, elastase-alpha 1-antitrypsin complex, tumor necrosis factor and interleukin-6) have been used to rule out a bacterial cause of fever.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunological methods for the detection of structural components and metabolites of bacteria and fungi in blood. 821 14

In vitro infection of freshly isolated human peripheral blood mononuclear cells (HPBMC) with Chlamydia pneumoniae was found to induce a production of tumour necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and interferon alpha (IFN-alpha). The secretion was dependent on the amount of infecting chlamydiae and most of it occurred during the first 12 to 24 h. Lipopolysaccharide (LPS) of Salmonella minnesota Rechemotype, used as a positive control for HPBMC activation, induced a release of TNF-alpha, IL-1 beta and IL-6, but not of IFN-alpha, similar to the effect of C. pneumoniae. Viable chlamydiae could not be recovered from HPBMCs infected immediately after their isolation, whereas HPBMCs which were cultured in vitro for 3 to 9 days before infection were able to maintain the growth of C. pneumoniae. Growth inside HPBMCs as well as induction of cytokine response may have a role in the pathogenesis of C. pneumoniae infection.
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PMID:Growth of Chlamydia pneumoniae in cultured human peripheral blood mononuclear cells and induction of a cytokine response. 887 18

Female mice bearing targeted mutations in the interleukin-6 or inducible nitric oxide synthase locus mounted effective immune responses following vaginal infection with Chlamydia trachomatis. Chlamydial clearance rates, local Th1 cytokine production, and host antibody responses were similar to those of immunocompetent control mice. Therefore, neither gene product appears to be critical for the resolution of chlamydial infections of the urogenital epithelium.
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PMID:Neither interleukin-6 nor inducible nitric oxide synthase is required for clearance of Chlamydia trachomatis from the murine genital tract epithelium. 948 25

Interleukin-6-deficient (IL-6(-/-)) knockout mice had significantly increased Chlamydia trachomatis levels in lung tissue and increased mortality compared to B6129F2/J controls early after intranasal infection. Gamma interferon production and chlamydia-specific antibody levels were consistent with a decreased but reversible Th1-like response in IL-6(-/-) mice. IL-6 is needed for an optimal early host response to this infection.
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PMID:A role for interleukin-6 in host defense against murine Chlamydia trachomatis infection. 971 22

The serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) were measured by enzyme immunoassays in 44 patients with Chlamydia (n = 13) or Mycoplasma (n = 14) pneumonia or influenza A infection (n = 17) and in 20 control subjects. The levels of IFN-gamma were raised in 29/44 patients. The concentrations of IL-6 were raised in 32/44 patients. Raised levels of TNF-alpha were seen in 26/44 but there was no significant difference between the levels of the different groups of patients. All three cytokines indicated clinical recovery when acute and convalescent samples from 10 patients with Chlamydia pneumonia were analyzed. IFN-gamma, IL6 and TNF-alpha are present in the circulation in the majority of patients with Chlamydia and Mycoplasma pneumonia and in influenza A infection. We suggest that repeated measurement of cytokines, such as IL-6, IFN-gamma and TNF-alpha, may be useful in the management of lower respiratory tract infections but further studies are needed to define the value of cytokine measurements in acute pneumonia.
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PMID:Cytokine responses in patients with pneumonia caused by Chlamydia or Mycoplasma. 973 Jul 97

C-reactive protein, a hepatic acute phase protein largely regulated by circulating levels of interleukin-6, predicts coronary heart disease incidence in healthy subjects. We have shown that subcutaneous adipose tissue secretes interleukin-6 in vivo. In this study we have sought associations of levels of C-reactive protein and interleukin-6 with measures of obesity and of chronic infection as their putative determinants. We have also related levels of C-reactive protein and interleukin-6 to markers of the insulin resistance syndrome and of endothelial dysfunction. We performed a cross-sectional study in 107 nondiabetic subjects: (1) Levels of C-reactive protein, and concentrations of the proinflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, were related to all measures of obesity, but titers of antibodies to Helicobacter pylori were only weakly and those of Chlamydia pneumoniae and cytomegalovirus were not significantly correlated with levels of these molecules. Levels of C-reactive protein were significantly related to those of interleukin-6 (r=0.37, P<0.0005) and tumor necrosis factor-alpha (r=0.46, P<0.0001). (2) Concentrations of C-reactive protein were related to insulin resistance as calculated from the homoeostasis model assessment model, blood pressure, HDL, and triglyceride, and to markers of endothelial dysfunction (plasma levels of von Willebrand factor, tissue plasminogen activator, and cellular fibronectin). A mean standard deviation score of levels of acute phase markers correlated closely with a similar score of insulin resistance syndrome variables (r=0.59, P<0.00005), this relationship being weakened only marginally by removing measures of obesity from the insulin resistance score (r=0.53, P<0.00005). These data suggest that adipose tissue is an important determinant of a low level, chronic inflammatory state as reflected by levels of interleukin-6, tumor necrosis factor-alpha, and C-reactive protein, and that infection with H pylori, C pneumoniae, and cytomegalovirus is not. Moreover, our data support the concept that such a low-level, chronic inflammatory state may induce insulin resistance and endothelial dysfunction and thus link the latter phenomena with obesity and cardiovascular disease.
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PMID:C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue? 1019 25

Inflammation and chronic infections may be important features in the pathogenesis of acute coronary syndromes. We describe 6 systemic markers of inflammation in patients with unstable angina or non-Q-wave myocardial infarction and the relations between these markers, seropositivity to chronic infections, and prognosis. C-reactive protein (CRP), serum amyloid A protein (SAA), fibrinogen, interleukin-6 (IL-6), neopterin, procalcitonin, and serum antibody levels to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus were measured on admission and 48 hours later. One-year clinical follow-up was performed. Plasma levels of acute phase reactants were all elevated on admission and increased further at 48 hours: CRP from 10.1 +/- 2.1 mg/L at baseline to 26.6 +/- 5.1 mg/L at 48 hours (p <0.001); SAA from 27.3 +/- 8.5 to 93.1 +/- 23.2 mg/dl (p <0.005); fibrinogen from 3.2 +/- 0.1 to 3.8 +/- 0.1 g/L (p <0.0001); whereas initial high levels of IL-6 tended also to increase from 9.8 +/- 2 to 15.3 +/- 3.1 pg/ml (p = NS). In contrast, neopterin and procalcitonin remained unchanged. We found no association between levels of each inflammatory marker and the serologic status. Furthermore, levels of inflammatory proteins in patients seronegative to all 3 agents were comparable to those of patients seropositive to 2 or 3 infectious agents. The composite end points of death, myocardial infarction, recurrent angina, or revascularization at 1-year follow-up did not differ according to the serologic status. Thus, in patients with acute coronary syndromes, the acute phase proteins increased over the first 2 days of hospitalization. This initial inflammatory reaction as well as the 1-year clinical outcome did not differ according to the initial serologic status of Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus.
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PMID:Effect of prior exposure to Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus on the degree of inflammation and one-year prognosis of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction. 1094 28

Inflammation is one of the most important mechanisms that contribute to coronary artery disease (CAD). One of the micro-organisms that is mentioned as a source of the inflammation is Chlamydia pneumoniae. In this study, we investigated the relationship between titres of IgG and IgA antibodies to C. pneumoniae and the clinical course, during hospitalisation and during an 18-month follow-up, in 211 patients admitted to hospital with unstable angina pectoris. Slightly more patients who were refractory during their hospitalisation were positive for C. pneumoniae antibodies than patients who could be stabilised by drug treatment (53 vs. 43%, for IgG and 16 vs. 11% for IgA, respectively)(n.s.). In logistic regression analysis no significant predictive values were observed for the relationship between antibody titres and clinical course. The antibody titres to C. pneumoniae were lower in the unstable angina patients who had plasma levels of interleukin-10 (IL-10) above 5 pg/ml than in the patients with levels below 5 pg/ml, and higher in smokers than in non-smokers. No associations were observed between antibody titres to C. pneumoniae and C-reactive protein (CRP), interleukin-6 (IL-6), age, total cholesterol levels, fibrin degradation products (FDP), plasminogen activator inhibitor-1 (PAI-1) and erythrocyte sedimentation rate (ESR). In conclusion, there was no significant association between antibody titres to C. pneumoniae and risk of events during hospitalisation and the 18-month follow-up period in patients admitted for unstable angina pectoris.
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PMID:Antibodies to Chlamydia pneumoniae and clinical course in patients with unstable angina pectoris. 1116 40

In a phase IV, open-label study, 25 patients with clinically stable chronic sinusitis and persistent maxillary sinus inflammation were treated for 14 days with clarithromycin 500 mg twice daily. Biopsy specimens of the maxillary sinus mucosa were obtained pretreatment and evaluated for macrophages (CD68), eosinophils (MBP), elastase, interleukin-6 (IL-6), IL-8, tumor necrosis factor-alpha (TNF-alpha), and activity of eosinophils (EG2), as well as edema score. Clinical signs and symptoms were assessed pretreatment, at the end of treatment, and 1 and 2 weeks later. Statistically significant reductions (P < or = .05) from pretreatment were observed for all markers of sinus mucosal inflammation, including CD68, EG2, elastase, IL-6, IL-8, TNF-alpha, and edema score, with a trend to decreased total eosinophil count. Improvement was observed for all clinical signs and symptoms of chronic sinusitis--sinus pain, sinus headache, nasal congestion, nasal discharge, and mucopurulent discharge--up to 14 days after the end of treatment. Cultures to evaluate persistent infection with Chlamydia pneumoniae showed negative results. Significant reductions in various markers of sinus mucosal inflammation support the role of clarithromycin in modulating immunologic responses. Improvement of clinical signs and symptoms in patients with chronic inflammatory sinusitis not meeting criteria for known or presumed bacterial infection was also noted up to 2 weeks after completion of a 14-day course of clarithromycin.
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PMID:Anti-inflammatory activity of clarithromycin in adults with chronically inflamed sinus mucosa. 1144 71


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