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)

Human diseases caused by the intracellular bacterium Chlamydia trachomatis include genital tract infections and blinding trachoma. Chlamydial infections are characterized by chronic inflammation and scarring, and development of such complications is thought to be immunologically mediated. In this study, we show that coculture of C. trachomatis (serovar L2) with human blood monocytes induced the production of interleukin-1 (IL-1), an important mediator of inflammation, tissue remodeling, and scarring. IL-1 was produced in response to UV-inactivated elementary bodies containing from 0.1 to 50 micrograms of protein per ml, with a maximal response at 5 to 10 micrograms/ml. IL-1 activity was detected by 6 h of incubation and was maximal by 24 h. Peak levels were maintained throughout 96 h of incubation. Rabbit antibody to human IL-1(alpha + beta) effectively neutralized the thymocyte-stimulating activity of the supernatants. The apparent molecular weight of chlamydia-induced IL-1 was 16,000, as determined by gel filtration on a Bio-Gel P-60 column. Isoelectric focusing yielded two peaks of activity, with pIs of 5.5 and 6.9. Neutralization studies with antisera against human IL-1 alpha and IL-1 beta showed that the acidic and neutral peaks corresponded to IL-1 alpha and IL-1 beta, respectively, with IL-1 beta predominating. Heat-killed chlamydiae, which are not internalized by monocytes, were effective IL-1 inducers, indicating that phagocytosis was not required for IL-1 induction. Purified C. trachomatis lipopolysaccharide was also an effective IL-1 inducer, suggesting that the response to intact organisms may be largely a response to chlamydial lipopolysaccharide. Finally, purified chlamydial major outer membrane protein induced low but detectable IL-1 activity.
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PMID:Chlamydia trachomatis-induced production of interleukin-1 by human monocytes. 278 36

DNAs from eight Chlamydia psittaci isolates (koala conjunctivitis, avian psittacosis, avian ornithosis, ovine abortion, ovine polyarthritis, sporadic bovine encephalomyelitis, and feline conjunctivitis) and one Chlamydia trachomatis isolate (lymphogranuloma venereum) were compared by restriction endonuclease and DNA probe analyses. Digestion with HindIII yielded a series of discrete fragments which allowed the differentiation of most isolates. A gene probe, pFEN207, which encodes the chlamydia-specific component of the lipopolysaccharide group antigen was used in Southern hybridizations. The probe was chlamydia specific and hybridized to a single BamHI fragment and multiple HindIII fragments in each isolate. The variation in size of the hybridizing fragments allowed easy differentiation of the isolates and may eventually lead to a meaningful subgrouping of the diverse group of disease agents presently included in the species C. psittaci.
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PMID:Comparison of Chlamydia psittaci isolates by restriction endonuclease and DNA probe analyses. 282 36

Paired sera from 40 male patients with acute myocardial infarction (AMI), 30 male patients with chronic coronary heart disease (CCHD), and 41 controls, matched for sex, age, time, and locality were investigated for antibodies to a novel type of Chlamydia sp, TWAR, and to chlamydial lipopolysaccharide (LPS) group antigen. 27 patients with AMI (68%), and 15 (50%) patients with CCHD had raised IgG (greater than or equal to 128) and/or IgA (greater than or equal to 32) titres in the microimmunofluorescence test with chlamydia TWAR. Both frequencies were significantly higher than in the controls (7, 17%). 26 (68%) of 38 patients with AMI also showed a significant seroconversion in enzyme immunoassay with LPS antigen; this response was absent in all patients with CCHD and all but 1 of the controls. Chronic chlamydial infection could be a factor in the pathogenesis of cardiovascular diseases.
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PMID:Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. 290 92

Peritoneal macrophages (M phi s) collected from Chlamydia psittaci 6BC-immune mice after intraperitoneal challenge with 10(6) 6BC (immune-boosted [IB] M phi s) were compared by various functional criteria with other in vivo- and in vitro-activated M phi populations. While casein-, protease peptone-, and thioglycolate (Thio)-elicited M phi s were equally susceptible to in vitro infection with 6BC, IB M phi s did not support chlamydial growth and M phi s from Mycobacterium tuberculosis BCG- or Listeria monocytogenes-sensitized mice exhibited intermediate susceptibility to infection. The resistance of IB M phi s was not due to the ingestion of fewer 6BC organisms, nor were these cells persistently infected, since chlamydiae could not be recovered from infected IB M phi s after in vitro infection, even after extended incubation times. In contrast, Thio M phi s stimulated in vitro with gamma interferon (IFN-gamma), with or without lipopolysaccharide, resulted in cells that exhibited chlamydiastatic activity which was lost shortly after IFN-gamma was removed from the culture medium. Conversely, the antichlamydial activity of IB M phi s was stable over time but not through the production of autostimulatory cytokines, as evidenced by the lack of stimulation of Thio M phi s to restrict 6BC replication in coculture experiments. IB M phi s exhibited enhanced oxidative activity, but anti-IFN-gamma antibody did not abrogate this response. IB M phi s were recovered only from immunized mice that survived an otherwise lethal 6BC intraperitoneal challenge. These cells appear to be important for development of protective immunity to chlamydiae, and evidence suggests that stimulation by cytokines other than IFN-gamma (with or without lipopolysaccharide) is required for the observed heightened in vivo activation.
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PMID:In vivo-activated mononuclear phagocytes and protective immunity to chlamydiae in mice. 313 Dec 46

A mu-capture enzyme-linked immunosorbent assay (ELISA) for detecting chlamydia-specific IgM was developed by use of the heat stable, lipopolysaccharide group-specific antigen and an alkaline phosphatase-labelled anti-chlamydia group-specific monoclonal antibody conjugate. The test was used to study the serological response in chlamydial respiratory tract infection among patients with acute respiratory tract symptoms in Cambridgeshire during the past 7 years. Results were compared with those of the complement fixation test (CFT) in routine use as well as those of a whole inclusion indirect immunofluorescence (WIF) test for IgM. Correlation between results of the mu-capture ELISA and those of the WIF test was 87.5%. The percentage of patients in whom specific IgM was found fell with increasing age. This may be due to lack of recall of IgM as a response to reinfection. Chlamydia-specific IgM was more likely to be detected when the CFT titre was greater than or equal to 64 and was rarely detected more than 6 months after the onset of symptoms. However, several patients less than 20 years of age were found to have specific IgM with CF antibody titres less than 64. We have found the mu-capture ELISA a useful test for the diagnosis of respiratory tract chlamydial infections, particularly in younger patients.
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PMID:The development and evaluation of a mu-capture ELISA detecting Chlamydia-specific IgM. 318 20

The sensitivity and specificity of an immune dot blot test (IDBT), which relies on a 125I-labeled genus-specific monoclonal antibody to detect the Chlamydia lipopolysaccharide (LPS) antigen, were improved by pretreatment of specimens with proteinase K. This enzyme destroys protein A and therefore eliminates false-positive reactions caused by the presence of Staphylococcus aureus. Proteinase K treatment also improved the ability of the assay to detect the Chlamydia LPS antigen. When the improved IDBT was compared with culture for detection of C. trachomatis in 1,394 urogenital specimens obtained from a genitourinary medicine clinic, the overall sensitivity was 96%, and LPS antigen was detected in 76 of 83 (92%) specimens that yielded less than 10 inclusions in culture. The specificity and positive and negative predictive values of the test were 97, 81.5, and 99%, respectively. Of 123 conjunctival swabs, 7 were positive by both tests and 4 swabs were positive only by IDBT. This improved IDBT provides a simple, reliable alternative to culture for the detection of C. trachomatis in urogenital and conjunctival specimens.
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PMID:Sensitive immune dot blot test for diagnosis of Chlamydia trachomatis infection. 318 26

The purpose of this investigation was to determine the relative roles of the humoral and cell-mediated immune responses in the resolution of chlamydial genital infection of mice and resistance to reinfection. To this end, female BALB/c mice were rendered B cell deficient by treatment with heterologous anti-immunoglobulin M (IgM) serum from birth. Controls were similarly treated with either normal serum or phosphate-buffered saline. Before inclusion in each experiment, anti-IgM-treated mice were screened for the absence of IgM in serum and for the presence of cell-mediated immune responses. In addition, spleen cells from anti-IgM-treated mice responded to concanavalin A and phytohemagglutinin but not to lipopolysaccharide. By these criteria, mice were designated B cell deficient. B-cell-deficient mice and controls were inoculated intravaginally with a suspension of mouse pneumonitis agent (MoPn), a Chlamydia trachomatis biovar. All B-cell-deficient mice resolved the infection. Additionally, no significant difference was seen in the course of the infection in B-cell-deficient mice when compared with controls. In contrast to control mice, B-cell-deficient mice displayed no detectable antibody responses to MoPn in serum or in genital secretions. However, both B-cell-deficient mice and controls developed delayed-type hypersensitivity and T-cell proliferative responses to MoPn. When challenged 53 days after primary infection, no significant difference was seen in the resistance of B-cell-deficient mice to reinfection when compared with that of the controls. These data indicate that cell-mediated immune mechanisms play an important role in the resolution of and resistance to chlamydial genital infection in this model.
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PMID:Resolution of chlamydial genital infection in B-cell-deficient mice and immunity to reinfection. 325 86

Chlamydial lipopolysaccharide (LPS) agglutinated mouse and rabbit erythrocytes but not human, guinea pig, or pronghorn antelope erythrocytes. Hemagglutination was not specific for Chlamydia spp., as rough LPSs from Coxiella burnetii and Escherichia coli also agglutinated erythrocytes from the same animal species. Nonagglutinated and agglutinated erythrocytes bound equivalent amounts of LPS, indicating that hemagglutination was not due to a specific interaction of chlamydial LPS with erythrocytes. Thus, hemagglutination by chlamydial LPS is not mediated by specific receptor-ligand interactions but is a property of the altered surface of the LPS-coated erythrocytes.
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PMID:Chlamydial hemagglutinin identified as lipopolysaccharide. 330 20

The effects of oral immunization with a recombinant vaccine expressing chlamydial lipopolysaccharide (LPS) on subsequent ocular challenge with Chlamydia trachomatis were studied in cynomolgus monkeys. Groups of four or five monkeys were given an oral vaccine containing 5 X 10(8) parent or recombinant Escherichia coli on days 0, 14, and 35 and were challenged with either 2 X 10(3) or 5 X 10(3) inclusion forming units of viable purified elementary bodies on day 42. On clinical and microbiologic grounds, oral immunization failed to protect monkeys against subsequent ocular challenge. Antichlamydial IgG or IgA antibodies were not induced by oral vaccination, and the antibody response following ocular challenge was similar in vaccinated and nonvaccinated animals. Paradoxically, however, while nonvaccinated control animals developed antibodies against chlamydial LPS detectable by immunoblotting after chlamydial challenge, the LPS vaccinated animals did not. This study demonstrates that the oral recombinant vaccine expressing chlamydial LPS was ineffective in protecting against chlamydial eye infection and strongly suggests that chlamydial LPS may not be an important antigen for protective immunity against chlamydia.
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PMID:Attempted oral immunization with chlamydial lipopolysaccharide subunit vaccine. 330 60

Antigens of the immunotype 1 strain B-577 of Chlamydia psittaci, which were separated by SDS-PAGE and electrophoretically transferred to nitrocellulose membranes were used to probe sequential serum samples of cattle with experimentally induced or naturally occurring chlamydial infections. Applying IgG1- and IgG2-specific markers in an enzyme immunoassay procedure, a predominance of IgG2 reactions with different proteins was determined. The interaction of IgG1 with antigens such as the genus-specific lipopolysaccharide and the major outer membrane protein was usually limited to periods immediately following overt clinical disease. Some other antigens like the 60,000 and 62,000 D proteins, for example, were recognized by both subclasses over the entire period of investigation. This indicates that it may be possible to determine the phase of infection through analysis of the IgG1 and IgG2 responses with the Western blot technique. The different IgG1 and IgG2 responses of cattle infected with different strains of Chlamydia psittaci as well as the diverse reactions of cattle from different herds with naturally occurring chlamydial infections further indicate that it may be feasible to distinguish the strains causing these chlamydial infections using different antigens in the Western blot technique. The results obtained by this method may have implications for the production of a subunit vaccine as well as for serodiagnostic purposes.
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PMID:Specific interaction of bovine IgG1 and IgG2 subclasses with different chlamydial antigens. 342 33


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