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)

A heavy load of bacteria, referred to as dental plaque, accumulates at the junction between the teeth and gum. Bacterial plaque may be considered to have three functional components: (a) cariogenic organisms, (b) organisms inducing gingival inflammation and periodontal disease, and (c) adjuvant and tolerizing agents, such as lipopolysaccharides, dextrans and levans. Sequential investigation of plaque accumulation in man has shown a correlation between gingival inflammation and both lymphocyte transformation and macrophage migration inhibition. An adjuvant effect of in vivo plaque accumulation was manifested by the enhancement of T lymphocytes in the mixed leucocyte culture reaction and of B lymphocytes, as shown by the increased response to lipopolysaccharide. It may be significant that a substantial component of bacterial plaque consists of dextrans and levans, produced by certain streptococci and actinomyces, and lipopolysaccharides from Gram-negative bacteria. These bacterial products are B cell mitogens which may have an adjuvant or tolerizing effect on immune responses. The relationships between immunogenicity, mitogenicity, adjuvanticity and tolerogenicity of lipopolysaccharides, levan and dextran have not been clearly defined. However, important variables of the polyglycans are the molecular weight, type of branching, negative charge, epitope density, degradability, dosage and the sequence between mitogen and antigen. Dental plaque in man is a focus of B cell mitogens and T cell antigens which may modulate the immune responses in such a way as to induce a protective response in the development of caries and a damaging response in periodontal disease.
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PMID:Immunological responses to bacterial plaque in the mouth. 34 20

A group of thirty-five mothers and their babies at parturition were examined by the in vitro lymphocyte transformation test to determine sensitization by oral bacterial antigens, B-cell mitogens and dental plaque. Lymphocytes from babies of sensitized mothers with gingival or periodontal disease gave the highest frequency (70 and 63%) and magnitude (mean stimulation index of 3.4 and 3.3) of response in cultures stimulated by Actinomyces viscosus and Veillonella alcalescens. However, IgM antibodies to V. alcalescens antigen were absent from cord sera. With one exception, stimulation of lymphocytes from babies of unsensitized mothers with clinically healthy gingiva was not found with these antigens. The response of cord lymphocytes from mothers with gingival or periodontal disease to antigens from oral bacteria, as compared with the response of cord lymphocytes from mothers with clinically healthy gingiva, seemed specific, since a corresponding difference in response to unrelated antigen PPD was not found. The response of cord and maternal lymphocytes to B-cell mitogens was also determined. Maternal lymphocytes responded in the following decreasing order of effectiveness: dextran sulphate, levan, lipopolysaccharide and dextran B1355; whereas cord lymphocytes were stimulated in the reverse order of effectiveness.
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PMID:Interdependence of in vitro responsiveness of cord and maternal blood lymphocytes to antigens from oral bacteria. 60 45

The inflammatory changes typical of periodontal disease are believed to involve immunological reactions, with bacteria being a potential source of the antigens inducing these reactions, with bacteria being a potential source of the antigens inducing these reactions. Various investigators have studied the ability of specific organisms to induce tissue changes in experimental animals, while others have examined human sera and tissues for the presence of antibodies reacting with particular organisms or their isolated antigens. The significance of these results is assessed, particularly with respect to the problem of antibody cross-reactivity. The antigens that could be involved in periodontal disease are discussed in terms of the difference in structure of Gram-positive and Gram-negative bacterial cells, with attention being drawn to those components that could occur extracellularly and thus diffuse into oral tissues. The antigen most studied is the lipopolysaccharide or endotoxin of Gram-negative cells which, through the mediation of complement, is a potential inflammatory agent.
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PMID:The potential role of bacteria and their antigens in periodontal disease. 107 Sep 72

We examined the production of interleukin-6 (IL-6) by human gingival fibroblasts (ATCC CRL 1292) stimulated with lipopolysaccharide (LPS) from Porphyromonas gingivalis and Escherichia coli, or supernatant of human peripheral blood adherent cell culture medium incubated in the presence of IL-1 and the same two LPS. Confluent monolayers of gingival fibroblasts were incubated with stimulants for 6 h at 37 degrees C in 5% CO2 and air. After removal of stimulants, the cell cultures were incubated for an additional 2 or 24 h in the same environment. At the end of the culture period, supernatants were collected and assayed for IL-6 activity by stimulatory IgG production with the human B-lymphoblastoid cell line CESS. The direct effect of LPS on IL-6 production by gingival fibroblasts was much weaker than the indirect one via IL-1 production by adherent cells. The stimulating effect of culture supernatants of adherent cells stimulated with LPS on IL-6 production by gingival fibroblasts was as effective as that of recombinant IL-1, when this latter was added at a concentration equivalent to that contained in the culture supernatant of adherent cells. These results suggest that, although gingival fibroblasts may be involved in the pathogenesis of chronic periodontal disease by the production of cytokines, such a role may not result from a direct stimulation by periodontopathic bacteria. The phenomenon is more likely to be mediated indirectly by IL-1 produced by infiltrating inflammatory cells.
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PMID:Direct and indirect effects of Porphyromonas gingivalis lipopolysaccharide on interleukin-6 production by human gingival fibroblasts. 132 99

There is substantial evidence in support of the existence of distinct clinical forms of human periodontal disease. Moreover, these different forms of periodontal disease may be associated with relatively distinct subgingival microflora, often involving microaerophilic or anaerobic Gram-negative bacterial species. Eikenella corrodens is a facultative Gram-negative bacillus which is a common inhabitant of the oral cavity and the intestinal and genital tracts. Its primary ecologic niche within the oral cavity appears to be dental plaque, both in periodontally healthy individuals and in periodontitis patients. However, E. corrodens is recognized as an infrequent human pathogen capable of causing extraoral infections, either as the sole infectious agent or as part of a mixed infection, its potential role in the etiology of periodontal disease is not well understood. E. corrodens is often present in the supra- and subgingival plaque of periodontally healthy subjects. On the basis of cross-sectional and longitudinal studies, E. corrodens appears to be somewhat more prevalent in subgingival plaque samples of periodontitis subjects than periodontally healthy individuals. However, the percentage of E. corrodens in the total cultivable microflora did not vary between the two groups. Microbiologic studies attempting to define the relationship between E. corrodens and periodontal disease assume that this species is essentially homogeneous and that all strains exhibit comparable pathogenic potential. However, E. corrodens exhibits 1) variable colony morphology, biochemical and serologic reactivity; 2) marked phenotypic diversity with respect to outer membrane protein and lipopolysaccharide structure; and 3) marked diversity in the restriction patterns of total genomic DNA. Thus, it is possible that a limited number of clones of E. corrodens may be associated with periodontal disease and/or extraoral infection, while other strains are relatively harmless commensals. Additional studies, possibly employing strain-specific nucleic acid probes, may be required to define the role of E. corrodens as a human periodontal pathogen.
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PMID:Eikenella corrodens in human oral and non-oral infections: a review. 147 66

Gingival mononuclear cells from patients with adult periodontitis were cultured to determine the potential for IgG production. All samples (N = 27) showed IgG synthesis. Some samples demonstrated IgG synthetic activity over the entire period in culture, often with maximum synthesis after 8 days. Other samples showed IgG synthesis during the first half of the culture period and then little detectable production for the remainder. Cells were either untreated or treated with one of several different known mitogens during the culture period. Total IgG synthesis by peripheral blood lymphocytes was enhanced in the presence of pokeweed mitogen, E. coli lipopolysaccharide and killed. A. actinomycetemcomitans. In contrast, IgG synthesis by gingival cells in the presence of these same additives was significantly reduced when compared to gingival cell synthesis in the absence of mitogens; suggesting the presence of suppression in this system. These differences in responsiveness may be attributable to the unique combination of T cells found in the gingival tissues of patients with periodontal diseases. The patterns of IgG synthesis by gingival cells were different from those of peripheral blood cells from the same patient. This finding verified the distinctiveness of local immunoregulatory mechanisms in periodontal disease tissue from those found systemically.
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PMID:Diminished immunoglobulin synthesis after stimulation of mononuclear cells from periodontal disease tissue. 147 78

We have isolated 10 rat T-cell clones from the spleen or lymph nodes of seven different donors. These rats were immunized with 2-5 x 10(8) killed Actinobacillus actinomycetemcomitans (Aa) bacteria, injected either subcutaneously (s.c.) in complete Freund's adjuvant or intraperitoneally (i.p.) in saline. Clones studied to date have demonstrated a T-helper (Th) phenotype W3/13+, W3/25+, OX8- and OX22-. Clones were not stimulated in vitro by purified Aa-lipopolysaccharide (LPS) or heterologous Gram-negative bacteria, but proliferated when stimulated by bacteria representative of each of the three serological groups of Actinobacillus, indicating specificity for an Actinobacillus-common antigen other than LPS. One clone (A4) proliferated vigorously when stimulated with concanavalin A (Con A) in vitro, produced interleukin-2 (IL-2) and was provisionally classified as a Th1 type. This appears to be one of the few Th1-type rat clones reported. All other clones tested did not produce IL-2, exhibited B-cell help to some extent, did not induce delayed-type hypersensitivity (DTH) when injected into the footpads of naive rats along with the specific antigen, and were classified as Th2 type. Adoptive transfer of 10(6) cells of one Th2-type Aa-specific clone into syngeneic recipients resulted in a specific splenocyte in vitro response to Aa 12-14 weeks after cell transfer, indicating survival of cloned cells in recipient animals. The use of such clones in studies of experimental periodontal disease is discussed.
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PMID:Characterization of rat T-cell clones with bacterial specificity. 169 11

The purpose of this study was to examine whether Bacteroides (Porphyromonas) gingivalis fimbriae, an important structure involved in attachment of the bacteria to periodontal tissues, activate macrophages and subsequently induce gene expression and production of interleukin-1 (IL-1) in the cells. The fimbriae increased glucose consumption and lysozyme activity in BALB/c macrophages, both criteria of macrophage activation of peritoneal macrophages, in a dose-dependent fashion. A marked increase in the mRNA level of the c-myc gene, an oncogene, in the cells was observed after a 1-h treatment with the fimbriae, and the level decreased rapidly after 3 h. The fimbriae (4 micrograms of protein per ml) markedly induced IL-1 alpha and IL-1 beta gene expression in the cells and IL-1 production. The expression of IL-1 alpha and IL-1 beta genes measured in terms of specific mRNA increased 1 h after the start of treatment and peaked at 6 h. Such increased expression of IL-1 beta was also observed in C3H/HeJ mice, a lipopolysaccharide low-responder strain. The fimbriae stimulated transcriptional activity of IL-1 beta in the cells, but not that of IL-1 alpha. We also observed that fimbriae-induced IL-1 gene expression was not regulated by endogenous prostaglandin triggered by the fimbriae. Therefore, these observations suggest that B. gingivalis fimbriae may be involved in the pathogenesis of adult periodontal disease via triggering of IL-1 production by monocytes/macrophages in periodontal diseases.
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PMID:Bacteroides (Porphyromonas) gingivalis fimbriae activate mouse peritoneal macrophages and induce gene expression and production of interleukin-1. 170 18

A particle concentration fluorescence immunoassay has been modified into a bacterial concentration fluorescence immunoassay (BCFIA) to rapidly detect periodontopathic bacteria in human plaque samples. The BCFIA utilizes fluorescently tagged monoclonal antibodies (MAbs) directed against the lipopolysaccharide of selected gram-negative plaque bacteria. Microorganisms closely associated with periodontal disease that can be identified in plaque with the BCFIA include Porphyromonas gingivalis, Bacteroides intermedius, Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum, and Eikenella corrodens. Briefly, the procedure involved mixing a patient's plaque sample or other bacterial preparation with a species-specific fluorescein isothiocyanate-labeled MAb in a specialized microtiter plate. This mixture was incubated to allow binding of the MAb to its homologous bacteria. The bound and unbound fluorescent tagged MAbs were separated by filtration in the modified microtiter plate, and the total bacterial bound fluorescence was determined with a fluorimeter. The number of a specific bacterial species in a given plaque sample or other bacterial suspension was estimated by reference to a primary standard carried through the BCFIA. The lower detection limit of the BCFIA was 10(3) to 10(4) bacterial cells from single cultures of bacteria or 10(4) bacterial cells in mixed cultures. The coefficient of variation within and between plates for each of the five bacterium-specific MAbs in screening plaque for the periodontal pathogens was less than 10%. These results demonstrate that microbes in plaque can be used as the solid phase in the BCFIA to detect and quantitate MAbs associated with specific bacteria quickly and reliably.
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PMID:Fluorescence immunoassay for detecting periodontal bacterial pathogens in plaque. 176 86

The adherence of lipopolysaccharides (LPSs) from periodontal disease-associated bacteria to saliva-coated hydroxyapatite (S-HA) and serum-coated HA beads was examined by chromogenic Limulus activity (toxicolor test). Phenol-water extracted LPS preparations from Bacteroides intermedius, Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, Eikenella corrodens, and rough-type LPS from Escherichia coli adhered to S-HA and serum-coated beads and agglutinated human erythrocytes. The adhered LPSs to S-HA and serum-coated HA beads were not removed by vigorous washing with distilled water. LPSs from Bacteroides (Porphyromonas) gingivalis strains and wild-type E. coli did not adhere to S-HA, serum-coated HA beads or show hemagglutinating activity. SDS-PAGE patterns stained with silver stain showed that LPSs adhered to S-HA, and serum-coated HA beads and erythrocytes possessed a distinct fast-migrating band similar to rough-type LPS. B. gingivalis LPSs possessed slow-migrating and repeating ladder bands similar to wild-type LPS.
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PMID:Adherence to experimental pellicle of rough-type lipopolysaccharides from subgingival plaque bacteria. 181 66


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