Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Periodontal disease is thought to be initiated by a bacterial infection and subsequently developed by immunopathological mechanisms thorough host-parasite interactions. The macrophage and lymphocyte are the major functional cell types in the lesion of the disease and participate in tissue destruction and alteration of the periodontal connective tissue as well as in host defense mechanisms. However, the detailed implications of macrophages in development of the disease is still unclear. The aim of this study was to gain more understanding of the functional role of macrophages in periodontal disease. In this study, we examined the inducing effects of sonicated extracts from some gram-negative and gram-positive bacteria associated with the pathogenesis of periodontal disease, including Bacteroides gingivalis, Fusobacterium nucleatum, Haemophilus actinomycetemcomitans, and Actinomyces viscosus, on activation of macrophage functions and IL-1 production by the macrophages from the mouse peritoneum. At a dose as low as 1 microgram/ml (dry weight) sonicated extracts from B. gingivalis induced an increase in acid phosphatase activity and in glucose consumption of mouse peritoneal macrophages in vitro. A significant increase in the acid phosphatase and in glucose consumption was observed in the cultures at 24 h and 48 h, respectively, after the addition of the sonicate. Sonicated extracts from A. viscosus, a gram-positive bacterium, as well as B. gingivalis, F. nucleatum, and H. actinomycetemcomitans, gram-negative ones, were able to induce the increase in acid phosphatase activity and in glucose consumption of the macrophages. These periodontopathic bacteria were found to strongly induce IL-1 production by the macrophages as early as 24 h after addition of the sonicates. A significant increase in the IL-1 production was observed at a dose of 1 microgram/ml of the sonicates. The inducing ability was equivalent to 1 microgram/ml Escherichia coli lipopolysaccharide. The highest production of IL-1 was observed in the macrophages treated with H. actinomycetemcomitans among these sonicates. Sonicated extracts from both gram-negative and gram-positive bacteria were able to induce the IL-1 production by macrophages from C3H/HeJ mice, which are LPS low-responders. These results suggest that periodontopathic bacteria have potent ability to induce macrophage activation and IL-1 production and that the activated macrophages may play an important role in development of periodontal disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Inducing effect of periodontopathic bacteria on activation of macrophage functions and production of interleukin-1 by mouse peritoneal macrophages]. 260 96

The present study was designed to investigate the effect of membrane proteoglycans (MPG) from Klebsiella pneumoniae on the function of human natural killer (NK) cells. MPG combined with bacterial ribosomes from Klebsiella pneumoniae, Streptococcus pneumoniae, Streptococcus pyogenes and Haemophilus influenzae, constitute a bacterial immunomodulator (MS D 53), currently in clinical use. Human peripheral blood lymphocytes (PBL) exposed in vitro to MPG or MS D 53 for 20 h showed enhanced NK cytotoxicity. Augmentation of NK cytotoxicity depended upon a direct effect on NK cells, inasmuch as these compounds were also effective on highly purified large granular lymphocytes (LGL). We also studied the effects of MPG on non-cytotoxic functions of NK cells, namely in vitro locomotion and production of IL-1. MPG (and MS D 53) induced IL-1 release in LGL. Moreover, MPG-treated LGL showed enhanced locomotory activity, as assessed by measuring the penetration into nitrocellulose filters. The capacity of MPG (and MS D 53) to activate cytotoxic and noncytotoxic functions of NK cells may contribute to enhancement of nonspecific resistance in vivo after treatment with this agent.
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PMID:Stimulation of cytotoxic and non-cytotoxic functions of natural killer cells by bacterial membrane proteoglycans and ribosomes. 278 90

Crude endotoxin preparations from Haemophilus actinomycetemcomitans and Bacteroides gingivalis showed activity in the two principal bio-assays for interleukin 1--the lymphocyte activating factor assay and stimulation of chondrocyte collagenase synthesis. Lipopolysaccharides purified from the crude endotoxins had reduced activity in the chondrocyte collagenase assay. The activity of the endotoxins may be due to synergic interaction between their lipopolysaccharides and other, as yet unidentified, bacterial components.
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PMID:The role of lipopolysaccharides in endotoxin-induced thymocyte proliferation and chondrocyte collagenase synthesis. 282 88

Whole Gram-negative bacteria associated with juvenile and adult periodontitis, and their respective extracted lipopolysaccharides (LPS), were tested for the ability to activate quiescent human peripheral blood monocytes. All pathogenic Gram-negative bacteria and all LPS tested were able to induce the production of significant amounts of IL-1 and TNF, monokines known to induce osteoclastic bone resorption. Haemophilus segnis, which has not been associated with any form of periodontal disease, did not activate monocytes. Purified LPS from Actinobacillus actinomycetemcomitans Y4 was able to elicit IL-1 and TNF release at a threshold concentration of 1-10 ng/mL. To examine the mechanism whereby whole bacteria activated monocytes, we added polymixin B in culture with glutaraldehyde-fixed bacteria to bind LPS. This resulted in the abrogation of IL-1 and TNF production. To compare the effects of Gram-positive oral bacteria on monocytes, we also tested Staphylococcus epidermidis and the Gram-positive amphipathic equivalent of LPS, lipoteichoic acid (LTA) extracted from Staphylococcus aureus bacteria. Whereas whole Gram-positive bacteria had no stimulatory effect on monocytes, LTA induced IL-1 and TNF production at a concentration range equivalent to that of the LPS. These results indicate that monocytes are activated by free LPS or LPS bound to Gram-negative pathogenic periodontal bacteria to produce monokines which may contribute to the destruction of periodontal bone.
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PMID:Production of interleukin-1 and tumor necrosis factor by human peripheral monocytes activated by periodontal bacteria and extracted lipopolysaccharides. 326 3

Intracisternal or intraarticular inoculation of rabbit recombinant interleukin (IL)-1 beta and rabbit tumor necrosis factor-alpha combined with IL-1 receptor antagonist (IL-1RA) and soluble tumor necrosis factor receptor (sTNFR), respectively, produced significantly less inflammation in rabbits than after inoculation of these cytokines alone. In contrast, when Haemophilus influenzae type b (Hib) or Hib lipooligosaccharide (LOS) was given intraarticularly with IL-1RA, sTNFR, or the combination, there was no significant or consistent modulation of synovial inflammation and cartilage proteoglycan degradation. In the experimental meningitis model, IL-1RA and sTNFR did not significantly reduce the meningeal inflammatory response associated with intracisternal inoculation of Hib LOS. These data indicate that specific cytokine inhibitors (sTNFR and IL-1RA) may not be effective in modulating inflammation induced by a broad inflammatory stimulus such as gram-negative bacteria or their products and suggest caution in using them to treat these infectious conditions in humans.
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PMID:Effect of interleukin-1 receptor antagonist and soluble tumor necrosis factor receptor in animal models of infection. 779 56

A deregulated expression and/or release of large amounts of inflammatory cytokines such as IL-1 and TNF-alpha accounts for most pathophysiological events in a variety of systemic inflammatory diseases, the effect being mediated by the interaction of these cytokines with their respective receptors. IL-1 receptor antagonist (IL-1Ra), mainly produced by monocytes/macrophages, is an inhibitor of IL-1 activity. The present study shows that human serum IgA induces significant IL-1Ra release in human peripheral blood mononuclear cells and adherent monocytes. IgA induced higher levels of IL-1Ra than Haemophilus influenzae type b (Hib) expressing lipopolysaccharide (LPS), purified LPS or phorbol myristate acetate (PMA), without induction of IL-1 beta release, and even inhibited LPS-induced IL-1 beta release. Induction of IL-1Ra by IgA could be detected both at the mRNA and protein levels in resting and activated monocytes. Ligation of Fc alpha R with MoAb My-43 or treatment with human serum IgA induced protein tyrosine phosphorylation in human monocytes, and herbimycin A, a specific inhibitor of protein tyrosine kinase activity, inhibited IgA-induced IL-1Ra production, suggesting that Fc alpha R-mediated induction of tyrosine phosphorylation is required for the IgA-induced stimulation of IL-1Ra release. In addition, triggering of Fc alpha R with MoAb specifically down-regulated TNF-alpha and IL-6 release in human monocytes activated with Hib. By the induction of IL-1Ra and down-regulation of the release of inflammatory cytokines such as IL-1 beta, TNF-alpha and IL-6, interaction of IgA with human monocytes may actively contribute to the regulation of the inflammatory response.
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PMID:Anti-inflammatory properties of human serum IgA: induction of IL-1 receptor antagonist and Fc alpha R (CD89)-mediated down-regulation of tumour necrosis factor-alpha (TNF-alpha) and IL-6 in human monocytes. 880 46

Recent studies have demonstrated the presence of inflammatory cytokines such as IL-1 beta, TNF-alpha, IL-6, and IL-8 in the middle ear effusion (MEE) of patients with otitis media with effusion (OME). IL-1 beta is known to be produced from macrophages and monocytes in an early stage of inflammation by stimulation with microorganisms and endotoxins. Also, these studies have shown that endotoxins frequently are found in MEE and can induce OME in experimental animal model. These findings suggest that endotoxins in MEE cause a chain reaction of cytokines through IL-1 beta. However, the precise role of IL-1 beta in the pathogenesis of OME has not yet been clarified. In the present study, a murine model of OME was developed by intra-tympanic injection with endotoxin or recombinant mouse IL-1 beta (rIL-1 beta) and the effects of IL-1 beta on the production of MEE were investigated. OME was induced in specific pathogen-free male BALB/c mice by intra-tympanic inoculation with endotoxin purified from nontypeable Haemophilus influenzae or with rIL-1 beta. The presence of MEE in the subjects was observed through the ear drum under a microscope and samples of MEE were collected by aspiration and washing with phosphate-buffered saline. The concentrations of IL-1 beta in each sample of MEE were determined by ELISA and the histological changes were compared. The mice inoculated with endotoxin showed signs of the production of MEE and it was noted that the levels of IL-1 beta in MEE were significantly increased on day 3. Intra-tympanic inoculation with rIL-1 beta also produced MEE and these cytological findings of MEE as well as the histological findings of middle ear mucosa were similar to those found in the endotoxin-induced OME. Further, the influence of anti-IL-1 receptor antibodies on the production of OME was examined 3 days after intra-tympanic injection with anti-IL-1 receptor antibodies together with endotoxin or rIL-1 beta. The incidence of OME was lower in mice injected with anti-IL-1 receptor antibodies than that in mice injected with endotoxin or rIL-1 beta only. These findings suggest that IL-1 beta may play an important role in the pathogenesis of OME.
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PMID:[The role of IL-1 beta in murine model of otitis media with effusion]. 979 75

In an ongoing prospective study, IL-1 concentrations were measured in 78 children (aged 3-36 months) with acute otitis media receiving antibiotics. Middle ear fluid IL-1 concentrations were determined using ELISA kits. Ninety-eight middle ear fluid samples were obtained by tympanocentesis at enrollment (day 1) and 43 samples were collected on days 4-5. Ninety-two pathogens were isolated in 77/98 samples obtained on day 1: 55 Haemophilus influenzae, 34 Streptococcus pneumoniae, 2 Moraxella catarrhalis and 1 Streptococcus pyogenes. Among 37 paired samples initially culture-positive, eradication of the pathogen was achieved on day 4-5 in 20 while pathogens were still present in 17. On day 1, IL-1 was detected in 61/77 (79%) culture-positive samples vs 9/21 (43%) culture-negative ones (P = 0.003). The mean +/- SD middle ear fluid concentration of IL-1 on day 1 was significantly higher in culture-positive (316 +/- 508 pg/ml) than in culture-negative samples (111 +/- 245 pg/ml) (P = 0.01). When paired samples were evaluated, IL-1 decreased on days 4-5 in 13/20 (65%) ears where bacterial eradication was achieved, but also in 11/19 (58%) with persistent or new infection. The mean IL-1 concentrations decreased on days 4-5 in the 20 samples from ears where bacterial eradication was achieved (330 +/- 460 vs 118 +/- 294 pg/ml, P = 0.1) but also in the 17 samples where it was not (465 +/- 660 vs 232 +/- 289 pg/ml, P = 0.02). No significant differences were found between day 1 and days 4-5 in the mean IL-1 concentrations measured in patients with H. influenzae vs S. pneumoniae or concomitant H. influenzae and S. pneumoniae. It was concluded that: 1) IL-1 was detected in the middle ear fluid of most patients with acute otitis media; 2) significantly higher IL-1 concentrations were found in patients with culture-positive than in those with culture-negative acute otits media; 3) IL-1 concentrations decreased on days 4-5 of antibiotic therapy, whether the pathogen was eradicated or not.
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PMID:Dynamics of interleukin-1 production in middle ear fluid during acute otitis media treated with antibiotics. 1037 27

To clarify the role of interleukin-1beta (IL-1beta) in the pathogenesis of otitis media with effusion (OME), we developed and investigated a murine model of this disease. Specific pathogen-free male BALB/c mice received intratympanic injections of 20 microg of endotoxin derived from nontypeable Haemophilus influenzae. Three days after injection, middle ear effusions were observed through the eardrum. Similar pathological changes were observed after inoculation with 100 ng of recombinant IL-1beta. Anti-IL-1 receptor antibodies inhibited the pathological changes induced by the endotoxin. In situ hybridization showed expression of IL-1beta messenger RNA in the epithelium of the middle ear mucosa. These results suggest that IL-1beta might be associated with endotoxin-induced inflammation in the middle ear and might play an important role in the induction of otitis media with effusion.
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PMID:Role of interleukin-1beta in a murine model of otitis media with effusion. 1140 50

During sepsis, endothelial cells are both a source and target of pro-inflammatory cytokines (e.g. IL-1alpha, IL-1beta, TNFalpha and others), which may be detrimental to vascular homeostasis. Our laboratory has demonstrated that Haemophilus somnus, a gram-negative pathogen of cattle that causes sepsis and vasculitis, and its lipooligosaccharide (LOS) induce caspases-3, -8 and -9 activation, and apoptosis of endothelial cells in vitro. In this study, we provide evidence that H. somnus LOS increases IL-1alpha and IL-1beta mRNA expression, and caspase-1 activation in endothelial cells. Addition of a caspase-1 inhibitor (YVAD), or incubation in a high extracellular potassium buffer (150 mM), reduced caspase-1 activation and significantly enhanced H. somnus LOS-mediated caspase-3 activation. Likewise, blocking the IL-1 type 1 receptor by addition of IL-receptor antagonist (IL-1ra) significantly enhanced LOS-mediated caspase-3 activation. Conversely, addition of exogenous recombinant bovine IL-1beta (100 ng/mL) to endothelial cells diminished LOS-mediated apoptosis. IL-1beta has been reported previously to protect numerous cell types from apoptosis by activating PI3 kinase/p-Akt signaling pathways. Addition of selective PI3 kinase inhibitors (e.g. wortmannin and LY294002) significantly enhanced LOS-mediated caspase-3 activation. Exposure of endothelial cells to IL-1beta or LOS increased pAkt protein as assessed by western blot. Overall, these results suggest that signaling through the IL-1 type 1 receptor diminishes H. somnus LOS-mediated apoptosis.
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PMID:Signaling through interleukin-1 type 1 receptor diminishes Haemophilus somnus lipooligosaccharide-mediated apoptosis of endothelial cells. 1612 94


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