Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 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

This study examined the phagocytic activity of rat peritoneal resident macrophages to determine the movement of macrophages in local inflammation in periodontal disease. We studied phagocytic activity by enzymelinked immunosorbent assay (ELISA) and used the peroxidase-anti-peroxidase soluble complex (PAP; soluble immune complex) as a marker in. We also determined the basic conditions of this examination and studied the effects of bacterial components and the supernatants of sonicated periodontopathic bacterias. We obtained the number of applied macrophages, the concentration of PAP to use and the incubation time. The phagocytic activity of macrophages was enhanced significantly by the bacterial components lipopolysaccharide (LPS) and muramyldipeptide (MDP). Phagocytic activity was also enhanced by the addition of the supernatant of sonicated Bacteroides gingivalis at 40 micrograms/ml (concentration of protein) and significantly suppressed at 320 micrograms/ml. Moreover, activity was significantly enhanced by the supernatant of sonicated Capnocytophaga suputigena at 40 micrograms/ml and 160 micrograms/ml, and suppressed by the supernatant of Fusobacterium nucleatum at a low concentration of protein (5 micrograms/ml). These results suggested that LPS of gram-negative bacteria's endotoxicity and MDP on pivotal structure of peptidoglycans, which are bacterial cell surface components, exerted an effect on phagocytic activity. It was further indicated that the phagocytic activity of macrophages varied with the effects of each periodontopathic bacteria.
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PMID:[Effects of periodontopathic bacterial components on phagocytic activity of rat peritoneal macrophages. Examination using ELISA]. 263 8

Fibroblasts of the periodontium may be involved in extracellular matrix degradation in response to inflammatory cytokines produced by mononuclear phagocytes. Interleukin 1 (IL1), one of these biologically-active agents, is produced by such cells when stimulated by lipopolysaccharide (LPS). Periodontal-ligament (PLF) and gingival fibroblasts responded to recombinant human IL1 beta and to media conditioned by LPS-stimulated mononuclear phagocytes by secreting prostaglandin E (PGE). This response was dose- and time-dependent. Stimulated gingival fibroblasts also produced about five- to ten-fold as much collagenolytic activity when compared to controls but PLF produced no more activity. On mixing the conditioned media from both fibroblast types, inhibitory activity was found in the PLF-culture medium. Thus gingival fibroblasts in particular may be involved in the pathogenesis of periodontal disease by responding to factors produced by inflammatory phagocytes.
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PMID:The effects of interleukin 1 on collagenolytic activity and prostaglandin-E secretion by human periodontal-ligament and gingival fibroblast. 326 Nov 62

This paper reports the activity associated with capsule-derived material and lipopolysaccharide extracted from Actinobacillus actinomycetemcomitans on connective tissue cells. The ability of lipopolysaccharide (LPS) to initiate inflammatory and destructive processes in the pathogenesis of periodontal disease was compared to that of capsular material (CM). The biological activities investigated were cytotoxicity to fibroblasts, stimulation of in-vitro bone resorption and Interleukin 1-like activities.
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PMID:The role of bacterial surface components in periodontal destruction. 327 Nov 18

Today, 10 black-pigmented Bacteroides (BPB) species are recognized. The majority of these species can be isolated from the oral cavity. BPB species are involved in anaerobic infections of oral and non-oral sites. In the oral cavity, BPB species are associated with gingivitis, periodontitis, endodontal infections and odontogenic abscesses. Cultural studies suggest a specific role of the various BPB species in the different types of infection. Bacteroides gingivalis is closely correlated with destructive periodontitis in adults as well as in juveniles. Bacteroides intermedius seems to be less specific since it is found in gingivitis, periodontitis, endodontal infections and odontogenic abscesses. The recently described Bacteroides endodontalis is closely associated with endodontal infections and odontogenic abscesses of endodontal origin. There are indications that these periodontopathic BPB species are only present in the oral cavity of subjects suffering from periodontal breakdown, being absent on the mucosal surfaces of subjects without periodontal breakdown. BPB species associated with healthy oral conditions are Bacteroides melaninogenicus, Bacteroides denticola and Bacteroides loescheii. There are indications that these BPB species are part of the normal indigenous oral microflora. Many studies in the past have documented the pathogenic potential and virulence of BPB species. This virulence can be explained by the large numbers of virulence factors demonstrated in this group of micro-organisms. Among others, the proteolytic activity seems to be one of the most important features. Several artificial substrates as well as numerous biological proteins are degraded. These include anti-inflammatory proteins such as alpha-2-macroglobulin, alpha-1-antitrypsin, C3 and C5 complement factors and immunoglobulins. B. gingivalis is by far the most proteolytic species, followed by B. endodontalis. Like other bacteria, the lipopolysaccharide of B. gingivalis has shown to be active in bone resorption in vitro and is capable in stimulating interleukin-1 production in human peripheral monocytes. Based on the well documented association with periodontal disease and the possession of relevant virulence factors, BPB species must be considered as important micro-organisms in the etiology of oral infections. B. gingivalis seems to be the most pathogenic and virulent species.
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PMID:The role of black-pigmented Bacteroides in human oral infections. 328 Jun 11

Actinobacillus actinomycetemcomitans is a fastidious, facultative gram-negative rod associated with endocarditis, certain forms of periodontal disease, and other focal infections. Human neutrophils have demonstrated bactericidal activity against A. actinomycetemcomitans, and much of the oxygen-dependent killing has been attributed to the myeloperoxidase-H2O2-halide system. However, the contribution of other neutrophil components to killing activity is obscure. Lactoferrin, an iron-binding glycoprotein, is a major constituent of neutrophil-specific granules and is also found in mucosal secretions. In this report, we show that human lactoferrin is bactericidal for A. actinomycetemcomitans. Killing activity required an unsaturated (iron- and anion-free) molecule that produced a 2-log decrease in viability within 120 min at 37 degrees C at a concentration of 1.9 microM. Besides exhibiting concentration dependence, killing kinetics were affected by minor variations in temperature and pH. Magnesium, a divalent cation thought to stabilize lipopolysaccharide interactions on the surface of gram-negative organisms, enhanced lactoferrin killing of A. actinomycetemcomitans, while other cations, such as potassium and calcium, had no effect. Our data suggest that lactoferrin contributes to killing of A. actinomycetemcomitans by human neutrophils and that it may also play a significant role in innate secretory defense against this potential periodontopathogen.
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PMID:Killing of Actinobacillus actinomycetemcomitans by human lactoferrin. 341 49

The chemical composition and immunobiological activities in vivo and in vitro of sodium dodecyl sulphate extracts (SDS-SE) derived from periodontopathic bacteria (three strains of Actinobacillus actinomycetemcomitans, two strains of Bacteroides gingivalis, and one strain of Fusobacterium nucleatum) were investigated. The main components of SDS-SE were protein and lipid, with negligible amounts of peptidoglycan and lipopolysaccharide. Immunopotentiating activity was detected in both delayed-type hypersensitivity and antibody formation against the elicitation of a protein antigen with the SDS-SE preparations of A. actinomycetemcomitans ATCC 29524 and B. gingivalis 381 and 1021. On the other hand the SDS-SE of A. actinomycetemcomitans ATCC 29522 enhanced only the induction of a delayed-type hypersensitivity response. All the SDS-SE preparations had mitogenic activity to splenocytes from BALB/c nu/nu, C3H/HeN and C3H/HeJ mice. Migration-stimulating activity for human peripheral blood monocytes was detected especially in the SDS-SE preparations of A. actinomycetemcomitans ATCC 29524 and Y4. All of the SDS-SE samples inhibited [3H]thymidine uptake in human gingival fibroblasts and caused degradation of the cells. The results suggest that the cell membrane components extractable with sodium dodecyl sulphate from periodontopathic bacteria are involved in the pathogenesis of periodontal disease.
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PMID:Chemical composition and immunobiological activities of sodium dodecyl sulphate extracts from the cell envelopes of Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Fusobacterium nucleatum. 365 33

Hot phenol-water-extracted lipopolysaccharide (LPS) from Bacteroides gingivalis 381 was purified by Sephadex G-100 chromatography with Tris buffer supplemented with sodium deoxycholate and EDTA (B-LPS). In the present study, B-LPS was examined for its ability to induce interleukin 1 (IL-1) production, a mitogenic response, and macrophage activation in LPS high-responder C3H/HeN and low-responder C3H/HeJ mice. A significant increase in IL-1 production was observed in C3H/HeN and C3H/HeJ peritoneal macrophages treated with various doses (1.0 to 50 micrograms/ml) of B-LPS. IL-1 production by C3H/HeN macrophages treated with B-LPS (10 micrograms/ml) was about seven times greater than that by C3H/HeJ macrophages. However, the IL-1 production induced by B-LPS (10 micrograms/ml) in C3H/HeN macrophages was four times lower compared with that induced by Escherichia coli O111 B4 LPS. Also, a significant increase in IL-1 production was found in human monocytes stimulated with B-LPS. That B-LPS-induced IL-1 exhibits some molecular weight heterogeneity was indicated from Sephadex G-75 gel filtration profiles. A significant, high mitogenic response by whole spleen cells with 1 X 10(5) to 5 X 10(4) cells of either mouse strain per well treated with B-LPS (10 to 50 micrograms/ml) was observed. However, the response of C3H/HeJ mice was less than that of the C3H/HeN strain. Also, glucose consumption assays indicated that enhanced macrophage activation occurred in C3H/HeN but not in C3H/HeJ mice treated with B-LPS. In light of recent studies showing that IL-1 stimulates bone resorption in a mouse calvaria system and collagenase production in fibroblasts, we suggest that B-LPS-induced IL-1 may play a significant role in the pathogenesis of adult periodontal disease.
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PMID:Functional role of interleukin 1 in periodontal disease: induction of interleukin 1 production by Bacteroides gingivalis lipopolysaccharide in peritoneal macrophages from C3H/HeN and C3H/HeJ mice. 387 85

The intracellular localization in 3T6 fibroblasts of Escherichia coli lipopolysaccharide (LPS) using the rapid avidin-biotin-immunoperoxidase technique at the electron microscopic level was studied. The role of bacterial endotoxin in the etiology of periodontal disease has been well documented previously. The purpose of the present study was to localize LPS within the cell, thereby determining which organelles concentrate the material and relate this to the cytologic pathophysiology. An increased concentration of LPS was found in the cell nuclei and, specifically, in association with nuclear chromatin and nucleoli. The concentration of LPS in the nucleus was directly related to the time of incubation, with some product appearing in that site within 2 minutes. There was no specific localization of endotoxin in mitochondria, lysosomes, Golgi, endoplasmic reticulum or ribosomes. These results imply that bacterial endotoxin may have a direct effect on nuclear components of fibroblasts. The relationship of these results to the etiologic mechanisms of periodontal disease is discussed.
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PMID:Intracellular localization of bacterial lipopolysaccharide using the avidin biotin complex method at the electron microscopic level. 389 6

Two separate species of lipopolysaccharide (LPS) from Bacteroides gingivalis 381 have been isolated. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated not only the heterogeneity of each species, but also that they represented high- and low-molecular-weight LPS entities. Although both contained the same carbohydrate and fatty acid components, the proportions of these differed between the LPS species. The direct effects of these two species in modulation of bone resorption and bone collagen and noncollagen protein synthesis have been examined. In a bone resorption assay, these two species stimulated 45Ca release from prelabeled fetal rat bones in a concentration range of 0.5 to 3.0 micrograms/ml. The two LPS species also elicited a 30 to 40% reduction in collagen protein formation at 10 micrograms/ml. Responses of the same order of magnitude were observed with LPS from Salmonella minnesota at 10 micrograms/ml. The higher-molecular-weight LPS species also significantly inhibited noncollagen protein formation. This is the first report that LPS from B. gingivalis 381, a suspected periodontal pathogen, inhibits bone collagen formation and, in conjunction with the bone resorption potency, further implicates LPS in alveolar bone loss associated with periodontal disease.
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PMID:Modulation of bone metabolism by two chemically distinct lipopolysaccharide fractions from Bacteroides gingivalis. 394 Sep 99


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