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)

Coxiella burnetii and Legionella micdadei are both gram-negative bacteria potentially responsible for identical clinical syndromes resembling upper respiratory infections. These infections, quite common in immunocompromised patients, are usually diagnosed by serology with a microimmunofluorescence assay. We found that 34.5% of Q fever patients had a significant titer of antibodies against L. micdadei. Cross-reactions involved immunoglobulin G antibodies and were demonstrated by a cross-adsorption study and protein immunoblotting. Western blot analysis performed after treatment with proteinase K indicated that cross-reactions were probably due to both protein and lipopolysaccharide antigens. It is critical that the existence of this cross-reaction be recognized, as misdiagnosis of either condition may lead to incorrect and ineffective treatment.
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PMID:Serological cross-reactions between Coxiella burnetii and Legionella micdadei. 906 57

In order to establish defined immunological parameters for Q fever infection models, a microtitre enzyme-linked immunosorbent fluorescence assay (ELISA) was used for the first time to analyse the humoral immune response of Balb/cJ and C57BL/6J mice after experimental infection with Coxiella burnetii strain 'Nine Mile' in phase I. The experimental infection evoked a seroconversion in all mice within 10 days. Typically, the immune response measured against the whole-cell antigen showed an early increase of immunoglobulin (Ig) M followed by a later increase of the IgG subclasses. The IgA was low during the entire investigation period. Within the IgG subclasses only IgG2a and IgG2b gained higher values, whereby C57BL/6J mice produced high IgG2b titres and significantly lower IgG2a titres. In contrast, Balb/cJ mice developed IgG2a and IgG2b at equal levels. The use of partial antigens of C. burnetii demonstrated that the dominating IgG2b reaction of the C57BL/6J mice was directed against the lipopolysaccharide (LPS) of C. burnetii. This reaction was almost absent in Balb/cJ mice. In contrast, the SP27 protein antigen did not evoke different IgG2b reactions within the two breeds. No significant influence was observed within the two breeds in regard to sex or between hormone synchronized and non-hormone synchronized animals.
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PMID:Analysis of immunoglobulin classes and subclasses in response to infection of Balb/cJ and C57BL/6J mice with Coxiella burnetii. 908 33

Lipopolysaccharides (LPSs) of 8 isolates of Coxiella burnetii from a variety of clinical and geographical sources could be divided into four groups based on molecular heterogeneity in silver-stained sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) profiles in the region of the 10 to 17 kDa. The lipopolysaccharide of group 1 was identified on isolates from acute Q fever patient, milk and tick. The three remaining groups were primarily found on isolates from human cases of chronic Q fever. These LPSs shared many antigenic epitopes, as determined by immunoblotting with mouse anti-C. burnetii antisera.
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PMID:Antigenic characteristic of the lipopolysaccharides of Coxiella burnetii isolates. 952 57

Coxiella burnetii, the agent of Q fever, enters human monocytes through alpha(v)beta(3) integrin and survives inside host cells. In addition, C. burnetii stimulates the synthesis of inflammatory cytokines including tumor necrosis factor (TNF) by monocytes. We studied the role of the interaction of C. burnetii with THP-1 monocytes in TNF production. TNF transcripts and TNF release reached maximum values within 4 h. Almost all monocytes bound C. burnetii after 4 h, while the percentage of phagocytosing monocytes did not exceed 20%. Cytochalasin D, which prevented the uptake of C. burnetii without interfering with its binding, did not affect the expression of TNF mRNA. Thus, bacterial adherence, but not phagocytosis, is necessary for TNF production by monocytes. The monocyte alpha(v)beta(3) integrin was involved in TNF synthesis since peptides containing RGD sequences and blocking antibodies against alpha(v)beta(3) integrin inhibited TNF transcripts induced by C. burnetii. Nevertheless, the cross-linking of alpha(v)beta(3) integrin by specific antibodies was not sufficient to induce TNF synthesis. The signal delivered by C. burnetii was triggered by bacterial lipopolysaccharide (LPS). Polymyxin B inhibited the TNF production stimulated by C. burnetii, and soluble LPS isolated from C. burnetii largely mimicked viable bacteria. On the other hand, avirulent variants of C. burnetii induced TNF production through an increased binding to monocytes rather than through the potency of their LPS. We suggest that the adherence of C. burnetii to monocytes via alpha(v)beta(3) integrin enables surface LPS to stimulate TNF production in THP-1 monocytes.
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PMID:alpha(v)beta(3) integrin and bacterial lipopolysaccharide are involved in Coxiella burnetii-stimulated production of tumor necrosis factor by human monocytes. 1099 70

A lipid A - deprived lipopolysaccharide (LPS) from Coxiella burnetii (C.b.) Priscilla strain in virulent phase I was separated by steric-exclusion chromatography and high performance liquid chromatography (HPLC). The isolated O-specific polysaccharide (PS) fractions were analyzed by different physico-chemical methods and showed noticeable differences in their overall composition. The antigenic potential of the PS fractions was evaluated by ELISA with animal and human sera and in comparison with those of the native C.b. LPSs and phase I and II C.b. Nine Mile stain cells of which the latter are routinely used in diagnosis of Q fever. The results indicate that the high molecular mass PS antigen SG501 could be used in ELISA for a sensitive and specific detection of anti-C.b. antibodies in the examined sera.
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PMID:Isolation and evaluation of Coxiella burnetii O-polysaccharide antigen as an immunodiagnostic reagent. 1177 96

Coxiella burnetii is the causative agent of Q fever. The bacterium is extremely infectious and is classified as a category biological weapon. A lipopolysaccharide I (LPS I) belongs to the main components of the C. burnetii outer membrane and its structure-function relationship studies are of potential interest. Size-exclusion chromatography revealed noticeable differences in distribution and chemical composition of the O-polysaccharide chains in LPS I. It is likely that C. burnetii is capable of synthesizing chemically distinct subclasses of O-specific polysaccharide molecules differing in their antigenic reactivities. Methylation-linkage analysis indicated the presence of terminal virenose (Vir), dihydrohydroxystreptose (Strep), and mannose (Man), 4-substituted Vir, and 4-substituted Man in the O-specific chain. Serological data indicate that Vir and Strep might be involved in the immunobiology of Q fever.
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PMID:Structural and functional characterization of the glycan antigens involved in immunobiology of Q fever. 1648 6

Coxiella burnetii is an obligate intracellular bacterium and the etiologic agent of the zoonotic disease Q fever. Symptomatic infection is normally characterized by flu-like symptoms; however, in some cases, a persistent infection can ensue that may reactivate months or years after initial exposure to cause chronic disease. The mechanisms by which this obligate parasite evades clearance by the host immune response during persistent infection are unknown. We have previously demonstrated that lipopolysaccharide (LPS) length is critical in determining the response of human dendritic cells (DC) to C. burnetii. Here, we investigated whether LPS chemotype affects DC maturation or activation. Immature human DC were infected with three virulent strains of C. burnetii (Nine Mile phase I, S, or Priscilla) that produce chemically distinct LPS molecules. None of these strains stimulated significant upregulation of cell surface markers of DC maturation. Moreover, these strains were equally deficient in inducing DC IL-12p70 production or p38 mitogen-activated protein kinase phosphorylation. Infection of DC by virulent C. burnetii without stimulating significant maturation or inflammatory cytokine production may be a mechanism of immune evasion that results in persistent infection of an otherwise immunocompetent host. Our data indicate that LPS chemotype is not a determinant of DC maturation or cytokine production in response to C. burnetii.
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PMID:Lack of dendritic cell maturation following infection by Coxiella burnetii synthesizing different lipopolysaccharide chemotypes. 1648 7

Coxiella burnetii, a gram-negative obligate intracellular bacterium, causes human Q fever and is considered a potential agent of bioterrorism. Distinct genomic groups of C. burnetii are revealed by restriction fragment-length polymorphisms (RFLP). Here we comprehensively define the genetic diversity of C. burnetii by hybridizing the genomes of 20 RFLP-grouped and four ungrouped isolates from disparate sources to a high-density custom Affymetrix GeneChip containing all open reading frames (ORFs) of the Nine Mile phase I (NMI) reference isolate. We confirmed the relatedness of RFLP-grouped isolates and showed that two ungrouped isolates represent distinct genomic groups. Isolates contained up to 20 genomic polymorphisms consisting of 1 to 18 ORFs each. These were mostly complete ORF deletions, although partial deletions, point mutations, and insertions were also identified. A total of 139 chromosomal and plasmid ORFs were polymorphic among all C. burnetii isolates, representing ca. 7% of the NMI coding capacity. Approximately 67% of all deleted ORFs were hypothetical, while 9% were annotated in NMI as nonfunctional (e.g., frameshifted). The remaining deleted ORFs were associated with diverse cellular functions. The only deletions associated with isogenic NMI variants of attenuated virulence were previously described large deletions containing genes involved in lipopolysaccharide (LPS) biosynthesis, suggesting that these polymorphisms alone are responsible for the lower virulence of these variants. Interestingly, a variant of the Australia QD isolate producing truncated LPS had no detectable deletions, indicating LPS truncation can occur via small genetic changes. Our results provide new insight into the genetic diversity and virulence potential of Coxiella species.
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PMID:Genetic diversity of the Q fever agent, Coxiella burnetii, assessed by microarray-based whole-genome comparisons. 1654 17

Coxiella burnetii, the etiological agent of Q fever, has two phase variants. Phase I has a complete lipopolysaccharide (LPS), is highly virulent, and causes Q fever in humans and pathology in experimental animals. Phase II lacks an LPS O side chain, is avirulent, and does not grow well in immunocompetent animals. To understand the pathogenicity of Q fever, we investigated the roles of immune components in animals infected with Nine Mile phase I (NM I) or Nine Mile phase II (NM II) bacteria. Immunodeficient mice, including SCID mice (deficient in T and B cells), SCIDbg mice (deficient in T, B, and NK cells), nude mice (deficient in T cells), muMT mice (deficient in B cells), bg mice (deficient in NK cells), mice deficient in tumor necrosis factor alpha (TNF-alpha(-/-) mice), and mice deficient in gamma interferon (IFN-gamma(-/-) mice), were compared for their responses to infection. SCID, SCIDbg, nude, and IFN-gamma(-/-) mice showed high susceptibility to NM I, and TNF-alpha(-/-) mice showed modest susceptibility. Disease caused by NM I in SCID, SCIDbg, and nude mice progressed slowly, while disease in IFN-gamma(-/-) and TNF-alpha(-/-) mice advanced rapidly. B- and NK-cell deficiencies did not enhance clinical disease development or alter bacterial clearance but did increase the severity of histopathological changes, particularly in the absence of B cells. Mice infected with NM II showed no apparent clinical disease, but T-cell-deficient mice had histopathological changes. These results suggest that T cells are critical for clearance of C. burnetii, either NM I or NM II, that IFN-gamma and TNF-alpha are essential for the early control of infection, and that B cells are important for the prevention of tissue damage.
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PMID:T cells are essential for bacterial clearance, and gamma interferon, tumor necrosis factor alpha, and B cells are crucial for disease development in Coxiella burnetii infection in mice. 1743 29

Coxiella burnetii is a macrophage-tropic, Gram-negative organism, which causes acute Q fever infection in humans. This zoonotic infection causes illness ranging from asymptomatic seroconversion to severe and protracted disease featuring hepatitis and pneumonia. Interactions between C. burnetii lipopolysaccharide (LPS) and host Toll-like receptors (TLR)-2 and -4 have been implicated in pathogen recognition, phagocytosis and signaling responses. Nonconservative single nucleotide polymorphisms in the coding regions of TLR-2 (Arg677Trp and Arg753Gln) and TLR-4 (Asp299Gly) have been found to correlate with mycobacterial infections and Gram-negative sepsis respectively. Associations between the TLR-2 and -4 polymorphisms, illness characteristics and immune response parameters were examined in subjects with acute Q fever (n=85) and comparison subjects with viral infections (n=162). No correlation was demonstrated between these polymorphisms and susceptibility to Q fever, illness severity or illness course.
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PMID:Polymorphisms in Toll-like receptors-2 and -4 are not associated with disease manifestations in acute Q fever. 1785 3


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