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Query: UMLS:C0023241 (Legionella)
6,990 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Legionnaires' disease (LD) bacterium is a gram-negative organism whose "endotoxicity" appears to differ in several respects from the classic endotoxicity generally associated with gram-negative bacteria. Discrepancies were noted between the high activity of LD bacteria in gelating limulus lysate in vitro and their low pyrogenicity in rabbits. Further in-vivo biologic tests indicated that LD bacteria were relatively weak in "endotoxicity". Analysis of LD bacterial cells and in their cellular fractions by gas-liquid chromatography indicated that LD bacteria did not contain hydroxy fatty acids commonly associated with lipid A of endotoxin. The branched-chain fatty acids that were characteristic of LD bacteria were associated with the cell envelope, and were readily extracted into organic solvents without prior saponification. The presence of 2-keto-3-deoxyoctonate in LD bacteria and cell extracts was detected by a microassay method but remains to be confirmed with gas-liquid chromatography and mass spectrometry. The active principle "endotoxicity" in LD bacteria may be a new type of bacterial lipopolysaccharide.
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PMID:"Endotoxicity" of the Legionnaires' disease bacterium. 43 47

Legionella pneumophila is an opportunistic intracellular pathogen that infects macrophages, both in vivo and in vitro. Tetrahydrocannabinol is a major psychoactive component of marijuana and can affect the functional activity of macrophages. In the present study, it was found that the treatment of macrophage cultures from permissive A/J mice with THC enhanced the growth of Legionella in these cells. Legionella grew much better in macrophages treated with low doses of THC, which caused no alteration in the number or viability of macrophages, as compared with growth in untreated cells. Furthermore, lipopolysaccharide-treated A/J mouse macrophages restricted the growth of Legionella, but this growth restriction was overcome by the addition of THC to LPS-treated macrophage cultures after infection. Thus, it is apparent that THC has the ability to enhance the growth of the intracellular opportunistic pathogen Legionella that grows in A/J mouse macrophages.
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PMID:Enhanced growth of Legionella pneumophila in tetrahydrocannabinol-treated macrophages. 130 98

The mechanism of the effects of lipopolysaccharide (LPS) on macrophages in terms of replication of intracellular facultative bacteria is unclear. It was found in the present study that the anti-Legionella pneumophila activity induced by LPS in macrophages from susceptible A/J mice was reversed in vitro by dibutyryl cyclic AMP (DcAMP). A 24-h pretreatment of murine thioglycolate-elicited macrophages with LPS resulted in an enhanced ability of these cells to inhibit the intracellular growth of L. pneumophila. This anti-L. pneumophila activity of macrophages induced by LPS was inhibited when DcAMP (10(-3) to 10(-5) M) was present during preincubation with LPS. The addition of DcAMP to the cultures was more effective before LPS treatment than after treatment. The effect of DcAMP was dose dependent. The secretion and production of acid phosphatase by LPS-activated macrophages were also inhibited by the addition of DcAMP before LPS treatment. Furthermore, the anti-L. pneumophila activity of macrophages induced by LPS could also be reversed in vitro by treatment with prostaglandin E2, colchicine, isoproterenol, theophylline, or hydrocortisone, all of which are known to increase the intracellular levels of cyclic AMP in various tissues. These observations indicate that the anti-L. pneumophila activity induced by LPS treatment can be modified by mechanisms involving cyclic nucleotide metabolism.
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PMID:Cyclic AMP inhibition of lipopolysaccharide-induced restriction of Legionella pneumophila growth in macrophage cultures. 131 22

Two long-chain fatty acids, 27-oxo-octacosanoic acid (28:0(27-oxo)) and heptacosane-1,27-dioic acid (27:0-dioic) were identified for the first time in phenol-chloroform-petroleum ether extracts of Legionella pneumophila, indicating that they are constituents of lipopolysaccharide. The fatty acids were characterised by combined gas-liquid chromatography/mass spectrometry and proton nuclear magnetic resonance spectroscopy. Moreover, minor amounts of 29-oxo-triacontanoic (30:0(29-oxo)) acid and nonacosane-1,29-dioic acid (29:0-dioic) as well as 27-hydroxy-octacosanoic acid (28:0(27-OH)) were present in the phenol-chloroform-petroleum ether extract.
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PMID:Identification of 27-oxo-octacosanoic acid and heptacosane-1,27-dioic acid in Legionella pneumophila. 142 93

The rapid development of biotechnological methods provides the potential of dissecting the molecular structure of microorganisms. In this review the molecular biology of chlamydia is described. The genus Chlamydia contains three species C. trachomatis, C. psittaci, and C. pneumonia which all are important human pathogens. Chlamydia is obligate intracellular bacteria with a unique biphasic life cycle. The extracellularly chlamydial elementary bodies (EB) are small, metabolic inactive, infectious particles with a tight outer cell membrane. After internalization into host cells the chlamydial structure changes, they transform to reticulated bodies (RB) which become larger, metabolically active, and start to replicate. Fourtysix hrs post infection RB reorganizes to EB followed by burst of the inclusion. The structure of the EB outer membrane differs from the membrane of gram-negative bacteria since it is highly cross-linked by S-S bridges. There are, however, also similarities to gram-negative cell walls. The chlamydial major outer membrane protein, Omp1, forms pores and is closely associated with lipopolysaccharide, LPS. LPS, however, is more loosely associated with Omp1 than in other gram negative bacteria since incubation of EB with antibodies against LPS will liberate it from the chlamydial surface. Therefore the surface localized LPS may be important for chlamydial survival. OMP1 varies between the different serovar of C. trachomatis. Several very conserved regions are separated by variable domains. The variable domains are very antigenic and are localized at the surface of EB. After chlamydial internalization into the host cell transition to RB starts. Some of the early proteins are DnaK-like and groEL-like heat-shock proteins. The chlamydial DnaK-like protein is very antigenic. Patient serum samples will recognize the chlamydial DnaK-like protein. From the determined DNA sequence the amino acid sequence was determined. It was 57% homologous to the Eschrichia coli DnaK protein. Also the GroEL-like protein is antigenic and very conserved. Factors of importance for pathogenicity of chlamydia have not yet been found. The adhesin(s) is unknown, and no factor of importance for the inhibition of fusion between phagosome and host cell lysosomes has been described. A protein similar to the mip gene product of Legionella pneumofila may be a possible candidate for a pathogenicity factor. Diagnosis of C. trachomatis infections has been done by chlamydia cultivation in tissue culture cells, by immunofluorescence and by ELISA. A new method based on the polymerase chain reaction (PCR) has been developed. As primers sequences from the common plasmid were used. This method has high sensitivity and specificity and does not require live chlamydia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The molecular biology and diagnostics of Chlamydia trachomatis. 152 83

Legionella pneumophila is a gram-negative bacterium capable of entering and growing in alveolar macrophages and monocytes. Complement and complement receptors are important in the uptake of L. pneumophila by human mononuclear phagocytes. The surface molecules of L. pneumophila that activate the complement system are unknown. To identify these factors, we investigated the effects of L. pneumophila lipopolysaccharide (LPS) on the classical and alternative complement pathways of normal human serum by functional hemolytic assays. Although incubation of LPS in normal human serum at 37 degrees C resulted in the activation of both pathways, complement activation proceeded primarily through the classical pathway. Activation of the classical pathway by LPS was dependent on natural antibodies of the immunoglobulin M class that were present in various quantities in sera from different normal individuals but were absent in an immunoglobulin-deficient serum obtained from an agammaglobulinemic patient. Additional studies using sheep erythrocytes coated with LPS suggested that the antibodies recognized antigenic sites in the carbohydrate portion of LPS. The ability of LPS to interact with the complement system suggests a role for LPS in the uptake of L. pneumophila by mononuclear phagocytes.
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PMID:Legionella pneumophila lipopolysaccharide activates the classical complement pathway. 161 44

Macrophages from A/J mice are permissive for growth of Legionella pneumophila, an intracellular opportunistic pathogen that grows preferentially in macrophages. Macrophages from other mouse strains are highly resistant to growth of Legionella. In the present study, it was found that macrophages from A/J mice are readily activated by pretreatment with lipopolysaccharide (LPS), so that the cells do not permit Legionella to replicate in vitro, as occurs when untreated macrophages from A/J mice are cultured with these organisms for 48 hr. The augmentation of Legionella growth inhibition by LPS-activated macrophages from nonpermissive BDF1 mice also occurred. After in vitro infection, there was a 1000-fold increase in the number of Legionella in A/J macrophages and approximately a 10-fold increase in BDF1 macrophages, but LPS treatment of macrophages from either strain resulted in marked growth restrictions. This suppression was both dose dependent as well as dependent upon the time of addition of the LPS to the macrophages. Furthermore, the lipid A component of LPS was found to be as effective as the intact LPS in activating macrophages to inhibit the intracellular growth of Legionella. Further studies concerning the mechanisms involved are clearly warranted and in progress.
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PMID:Enhanced growth restriction of Legionella pneumophila in endotoxin-treated macrophages. 161 9

Infection of peritoneal macrophages from susceptible A/J mice with Legionella pneumophila induced phosphorylation of a 76-kDa protein. The phosphorylation occurred when macrophages were infected with a virulent strain of L. pneumophila but did not occur when they were infected with an avirulent strain or with other bacteria such as either Pseudomonas aeruginosa or Salmonella typhimurium. Also, no phosphorylation of this protein was observed when macrophages were stimulated with either lipopolysaccharide or phorbol myristate acetate. However, phosphorylation did occur in macrophages infected with a virulent strain of L. pneumophila and treated with either erythromycin to inhibit growth or with cytochalasin D to inhibit uptake of L. pneumophila by macrophages. These results support the view that phosphorylation of this protein occurs during the early phases of interaction between L. pneumophila and macrophages. The role of this specific protein in the recognition, intracellular uptake, and growth of L. pneumophila in permissive macrophages remains to be clarified.
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PMID:Infection of macrophages with Legionella pneumophila induces phosphorylation of a 76-kilodalton protein. 163 15

Legionella pneumophila is a facultative intracellular pathogen which readily grows in human and guinea pig macrophages and in peritoneal exudate macrophages from A/J mice. Macrophage cultures capable of supporting the growth of Legionella can be used to test the potency of biologically active substances suspected of modulating host mechanisms of resistance to infection. Accordingly, this model was used to evaluate the influence of delta-9-tetrahydro-cannabinol (THC) on macrophage resistance to infection with an intracellular pathogen. Pretreatment of the macrophages with THC in the concentration range of 2.5 micrograms/ml (8 microM) to 5.0 micrograms/ml (16 microM) had little if any effect on the ability of the macrophages to either ingest or support the replication of Legionella. However, THC treatment of cells following Legionella infection resulted in increased numbers of bacteria recoverable from the macrophage cultures. Stimulation of the macrophage cultures with the activating agent lipopolysaccharide (LPS) was effective in reducing the ability of Legionella to grow in the cells. However, treatment of the LPS activated macrophages with THC resulted in greater growth of the Legionella in the cultures, indicating that the drug abolished the LPS induced enhanced resistance. These results demonstrate that THC treatment of macrophages following infection rather than before infection with Legionella promotes the replication of the bacteria within the macrophages. In addition, drug treatment suppresses the growth restricting potential of macrophages activated by LPS.
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PMID:Tetrahydrocannabinol treatment suppresses growth restriction of Legionella pneumophila in murine macrophage cultures. 165 Aug 75

Monoclonal antibody II-6-18 recognizes a serogroup-1-specific Legionella pneumophila antigenic determinant which has been shown to be virulence-associated. We previously reported the physicochemical characterization by means of a quantitative fluorometric assay of monoclonal antibody II-6-18 binding to L. pneumophila, and its implications concerning the nature of the antigen. We describe here the isolation and the purification of the antigen by chemical and immunological methods, followed by its partial chemical analysis. The results demonstrate that the epitope--an immunodominant carbohydrate which includes a fucosamine-like residue--is part of the cell wall lipopolysaccharide (LPS). It is localized in the polysaccharide moiety of the LPS which contains KDO, rhamnose, mannose, glucosamine and an unidentified aminodideoxyhexose X1, but no heptose. The aminodideoxyhexose X1 could be fucosamine and is probably the immunodominant residue in the epitope, localized, at least partially, at the end of the polysaccharide chain.
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PMID:Isolation, purification and partial analysis of the lipopolysaccharide antigenic determinant recognized by a monoclonal antibody to Legionella pneumophila serogroup 1. 209 60


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