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 purified lipopolysaccharide (LPS) isolated from the rickettsial agent of Q fever, Coxiella burnetii phase 1, possesses some of the in vivo and in vitro biological properties previously only associated with bacterial endotoxins. The Coxiella LPS is mitogenic for guinea pig leukocytes, induces non-specific resistance in mice to virulent Candida albicans, causes dermal Schwartzman reactions, and is positive by the limulus lysate assay.
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PMID:Mitogenic and protective activity associated with a lipopolysaccharide from Coxiella burnetii. 74 20

The lipopolysaccharide previously isolated from the rickettsial agent of Q fever, Coxiella burneti, phase I, has been further characterized. The sugar residues ribose, mannose, gluclose, D-glycero-D-mannoheptose, and L-glycerto-D-mannoheptose are present. Two sugars remain unidentified, one of which is a minor and the other a major constituent. Isomyristic, palmitic, and beta-hydroxymyristic acids are the major fatty acid residues of the 15 identified. The nature and content of other lipopolysaccharide constituents are presented.
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PMID:Further characterization of a lipopolysaccharide from Coxiella burneti. 97 47

The underlying mechanisms at the organismic, cellular and molecular levels that account for rickettsial pathogenesis are beginning to be revealed. In the case of Coxiella burnetii infection, relatively recent genetic and biochemical data, as well as drug susceptibility studies, indicate a correlation between isolate type and clinical disease--chronic or short-term acute. The use of cultured cells as model host systems has revealed that, indeed, different isolates from the major classified strains of C. burnetii cause different host cell responses. Use of this and other models (guinea pigs, mice) have revealed other characteristics and properties of the rickettsiae and the infected hosts and host cells that may account, in part, for acute disease and persistent infection culminating in chronic disease. The virulence factors involved apparently include the agent's surface lipopolysaccharide; other unidentified factors have not been excluded. Molecular cloning will play a major role in elucidating the roles of these factors and in identifying other virulence determinants.
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PMID:Pathogenesis of rickettsial infections emphasis on Q fever. 188 73

Sheep erythrocytes sensibilized with the lipopolysaccharide (LPS) extracted from Coxiella burnetii phase 1 cells were used in indirect haemolysis test (IHT). The test was highly sensitive and specific. Its use seemed reasonable when following the chronic course of Q-fever by serologic methods.
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PMID:Indirect haemolysis test in Q-fever. 198 47

Vaccination with an inactivated, whole cell, Q fever vaccine (Q-vax) induces lasting antibody conversion and a positive delayed-type hypersensitivity (DTH) skin reaction in about 60% of recipients but a long-lasting positive lymphoproliferative or mitogenic response to C. burnetii antigens with peripheral blood mononuclear cells (PBMC) in 85-95% of subjects. Analysis of the lymphoproliferative response to C. burnetii antigens has now been made by fractionation-reconstitution experiments with PBMC from vaccines, from past infections, and from healthy controls. The major contributor to the response in immune subjects proved to be the T lymphocyte. T cells were stimulated by both the phase I and phase II antigens of two prototype strains of C. burnetii and responses were greatly amplified by addition of IL-2. Similar T lymphocyte stimulation profiles were obtained with the 'Priscilla' strain of C. burnetii which represents a different biotype of Coxiella isolated from Q fever endocarditis; Q-vax is therefore likely to protect against endocarditis strains. Fractionation-reconstitution experiments with T and B cells from vaccines and subjects infected in the past, using various antigenic or haptenic fractions from C. burnetii indicate that protein, non-lipopolysaccharide components of the organism are responsible for the mitogenic response of immune T cells. However, the role of the lipopolysaccharide in the protective immunogen has still to be defined.
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PMID:Analysis of the cells involved in the lymphoproliferative response to Coxiella burnetii antigens. 207 May 64

The isotypic immune response of 16 individuals who developed Q fever pneumonia following exposure to an infected parturient cat was studied. The enzyme-linked immunosorbent (ELISA) test was used to detect IgM, IgA, and IgG antibodies to phase I and phase II Coxiella burnetii whole-cell antigens and to the phase I lipopolysaccharide. The indirect immunofluorescent antibody (IFA) test was also used to detect antibodies to phase I and phase II whole cells. None of the 16 subjects developed antibodies to the phase I lipopolysaccharide. The ELISA was more sensitive than the IFA test. IgM antibodies to phase II antigen were detectable by ELISA in 80% of the subjects at the time of onset of symptoms and were still present in 7 of the 8 tested at 32 weeks following the onset of symptoms. In all instances (ELISA: IgG, IgM; IFA: IgG, IgM) phase II antibodies developed earlier and reached higher levels than did phase I antibodies. The absence of antibodies to phase I lipopolysaccharide in acute Q fever combined with our unpublished findings of antibodies to phase I lipopolysaccharide in chronic Q fever suggests that this test may be used to distinguish acute from chronic Q fever.
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PMID:The immune response in a cat-related outbreak of Q fever as measured by the indirect immunofluorescence test and the enzyme-linked immunosorbent assay. 219 85

The antigenic structure of Coxiella burnetii is being investigated by identifying both external and internal cellular epitopes of the morphologic cell types. Both the phase I lipopolysaccharide (LPSI) and several surface proteins are candidates for the development of subunit multivalent vaccines. The protective efficacy of purified LPSI was demonstrated in A/J mice. The purified LPSI preparations contained residual peptides detected by amino acid analysis. Therefore, the protection afforded by LPSI may be, in part, due to the presence of peptides. The purification of proteins free of LPSI must be accomplished before the protective efficacy of proteins or peptides can be established. We have identified three proteins that are both antigenic and immunogenic, as indicated by either enzyme immunoassay, radioimmunoprecipitation, immunoblot assay, or lymphocyte transformation. A 62-kDa protein antigen encoded by the htpB gene of C. burnetii was analyzed for immunogenicity. The purified protein antigen was immunogenic, as it elicited specific antibodies and performed as recall antigen in lymphocyte stimulation assays. The antigen was not detected on the surface of phase I cells but was highly represented on the surface of phase II cells. Therefore, the protein may not be a good candidate for vaccine development. The diagnostic utility of the 62-kDa protein antigen lies in the fact that convalescent and chronic Q fever sera from human patients reacted with the antigen, whereas acute sera did not. Although the 62-kDa protein is a "common antigen," specific peptide-based diagnostic reagents may be useful in the detection of Q fever disease progression. A major surface protein (P1) of roughly 29.5 kDa was purified from the phase I Nine Mile (clone 7) strain. No LPSI was detected in the P1 preparation by three different LPSI monoclonal antibodies. Monoclonal antibodies prepared against P1 were effective in localizing the protein on the cell surface, in the cell wall, and associated with the peptidoglycan of large cells of C. burnetii. Small, pressure-resistant cells did not contain P1. Mice immunized with two 25-micrograms injections of LPSI produced antibodies against LPSI and phase I whole cells. No antibody was detected against phase II whole cells. Immunization with P1 induced antibody against the LPSI fraction and phase I and phase II whole cells. P1 was more effective than LPSI in reducing the number of infectious C. burnetii in the spleens of challenged mice. The gene encoding another protein (P2) recognized by P1 monoclonal antibodies was cloned and sequenced.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antigenic structure of Coxiella burnetii. A comparison of lipopolysaccharide and protein antigens as vaccines against Q fever. 237 63

Guinea pig endotoxicosis induced by lipopolysaccharide from Coxiella burnetii Nine Mile phase I stimulates phosphorylation of liver ribosomal protein S6, with a 50% increase at 12 h postinoculation. The responsible protein kinase (S6PK) has been partially purified from liver; its activity is independent of cyclic AMP and of Ca2+ plus phosphatidyl serine or diacylglycerol. The preparation has an apparent optimum concentration of 20 mM Mg2+, while Ca2+ and Mn2+ are each inhibitory at 2 mM. The apparent Km for ATP is 30 microM with intact ribosomes. Because of the central role of phosphorylation in metabolic regulation and a purported role of phosphorylated S6 in protein synthesis, the lipopolysaccharide-induced stimulation of S6PK suggests a significant regulatory role of such enzymes in the pathobiochemistry of Q fever infection and endotoxicosis.
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PMID:Endotoxicosis induced by Coxiella burnetii lipopolysaccharide stimulates a ribosomal protein S6 kinase: some properties of the partially purified enzyme. 280 43

Coxiella burnetii, the etiological agent of Q fever, possesses immunomodulatory activity which positively and negatively regulates host immune responses. We wish to determine the Coxiella strain differences and the chemical nature of cellular components suppressing lymphocyte responsiveness. The bacterial components responsible for the immunomodulatory activity are associated with phase I cells. In its natural state, the phase I cell-associated, immunosuppressive complex (ISC) was resistant to chemical and enzymatic treatment. The ISC was inactivated and rendered accessible by chloroform-methanol (CM) (4:1) extraction of phase I cells which produced a CM residue (CMRI) and CM extract (CME). The suppressive components in either CMRI or CME did not induce ISC activity in the host when injected separately. Reconstitution of the CMRI with CME prior to injection produced the same pathological reactions characteristic of phase I cells. The CMRI suppressive component was sensitive to alkali, acid, periodate, lysozyme, and neuraminidase, but resistant to lipase and protease. An active component of CMRI was attached to the cell matrix by disulphide bonds. The amphipathic, lipophilic, CME suppressive component was ubiquitously distributed in procaryotes and eukaryotes because ISC activity of CMRI was regained after association with reagent-grade lipids and different CMEs. The ISC was expressed by phase I strains with smooth lipopolysaccharide (LPS) but not by phase II strains with rough LPS. Phase I heart valve strains carrying significant amounts of rough LPS did not express all of the biological properties of the ISC. The LPS molecule induced immune enhancement without immunosuppression. Thus, expression of the ISC showed strain variation and may be under genetic control. The complete details of the chemical composition and active components of the ISC should prove useful for biological-response-modification studies.
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PMID:Immune modulation by Coxiella burnetii: characterization of a phase I immunosuppressive complex differentially expressed among strains. 317 Nov 7

A histologic, immunofluorescence, and electron microscopic study of the intracellular parasitism of Coxiella burnetii (the Q fever agent) in mouse lungs after intranasal challenge was undertaken. It was shown that this microorganism invades type I and, rarely, type II pneumocytes as well as pulmonary fibroblasts and histiocytes. The infectious process can be described as a focal intra-alveolar inflammation with the macrophages prevailing in the exudate. It is self-limited, with a complete resolution. The inflammation is associated with atelectases and with increased secretory activity by type II pneumocytes. Alveolar macrophages and granulocytes degrade C. burnetii. This degradation is followed by damage to and eventual disintegration of some macrophages and by damage to some bacterium-free pneumocytes and vascular endothelial cells in the vicinity of macrophages degrading organisms. The cell damage might be caused by lipopolysaccharide released from degraded organisms. The infectious process is also associated with the influx of T cells in the pneumonic foci, T-cell attachment to the macrophages degrading organisms, and fusion of some macrophages. These are considered a morphologic expression of cell-mediated immunity involved in the infectious process.
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PMID:Histologic, immunofluorescence, and electron microscopic study of infectious process in mouse lung after intranasal challenge with Coxiella burnetii. 329 Jan 7


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