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 total of 226 cultures of Vero cytotoxin-producing Escherichia coli O 157 isolated from humans was received by the PHLS Laboratory of Enteric Pathogens during the six month period January to June 1992. A record monthly total of 122 isolates was received in June. Ten phage types (PT) were identified during this period; PT 2 (45%) and PT 49 (21%) predominated. In addition, 27 human sera with antibodies to E. coli O 157 lipopolysaccharide (LPS) were examined from other cases during this period, making a total of 253 cases of infection associated with E. coli O 157.
Commun Dis Rep CDR Rev 1992 Nov 06
PMID:Vero cytotoxin-producing Escherichia coli O 157 in the United Kingdom. 128 37

Two out of five murine IgG3 anti-trinitrophenyl (TNP) monoclonal antibodies (mAb) obtained either by immunization with TNP-keyhole limpet hemocyanin (KLH) (CB1, CB5, CB6 and 4H10) or with dinitrophenyl-lipopolysaccharide (9A6), exhibited anti-IgG rheumatoid factor (RF) activity (CB6 and 4H10). The anti-IgG activity of these two anti-TNP RF was specifically inhibited by murine IgG as well as by the hapten TNP. In order to identify the structural basis for the anti-IgG activity, the nucleotide sequences encoding the VH and VL regions were determined. By comparing the V regions of the non-RF and RF anti-TNP mAb, it was found that one anti-TNP RF antibody, CB6, shares virtually identical VL and VH regions with two anti-TNP antibodies, CB1 and CB5, but markedly differs from these in the D region. Furthermore, the light chain framework region 2 (FR2) and FR3 of non-RF mAb, CB1, CB5 and 9A6, have amino acid sequences almost identical to those claimed for anti-IgG1 RF activity (Shlomchik et al., J. Exp. Med. 1986. 164: 407). Our findings suggest, at least in the case of CB6 mAb, the involvement of CDR, but not light chain FR residues, in IgG binding.
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PMID:Rheumatoid factor autoantibody-binding site: a molecular analysis using monoclonal antibodies with dual anti-TNP and anti-IgG activities. 225 89

New meningococcal vaccines are needed in the United Kingdom with some urgency. Almost all Neisseria meningitidis disease in this country is caused by serogroups B and C. Infants have the highest attack rates, but also make the poorest immunological responses to potential vaccines. The development of vaccines that protect infants is a significant challenge. A capsule-based serogroup B vaccine is unlikely to be successful in infants because the capsule is poorly immunogenic and the polysaccharide molecule mimics a human epitope. Without completely discounting capsule as an immunogen, alternate antigens are being considered for immunisation: outer membrane proteins (OMP), iron regulating proteins, and lipopolysaccharide. Vaccines based on OMP have been used in several phase 3 trials in South Africa, Cuba, Brazil, Norway, and Chile, in which two doses of vaccine were given. The Cuban and Norwegian vaccines have been compared in phase 2 trials in Iceland and Chile. Potential limitations are epitope heterogeneity and the theoretical ability of N. meningitidis to adapt even to hosts who have received polyvalent vaccines. A phase 2 trial of a hexavalent class 1 OMP vaccine is under way in Gloucester, with 100 babies receiving injections at 2, 3, and 4 months. Serogroup C vaccines have been developed from capsular polysaccharide but, unconjugated, these vaccines do not protect those under 2 years of age. Conjugate vaccines with C and AC polysaccharides are immunogenic in infants, but antibody titres may wane quickly.(ABSTRACT TRUNCATED AT 250 WORDS)
Commun Dis Rep CDR Rev 1995 Aug 18
PMID:Meningococcal vaccines for the United Kingdom. 767 May 76

In a one month period in the summer of 1993 a community outbreak of Escherichia coli O157 infection affected six children living within an area of 1.5 miles radius in south west London. Three children developed haemolytic uraemic syndrome, one of whom died. E. coli O157 phage type 2 was isolated from faeces in five cases and serological tests showed the sixth child had antibodies to E. coli O157 lipopolysaccharide. E. coli O157 phage type 2 was isolated from a faecal specimen from this child's mother who was a secondary case. Three of the cases, whose onset dates were within three days of each other, had all been exposed to a paddling pool where disinfection procedures were found to be inadequate. Samples of water taken from this pool contained E. coli, although not the O157 serotype. A fourth case had played at a different paddling pool in the three days before becoming ill. Action has been taken to improve disinfection procedures at municipal paddling pools in the London borough concerned.
Commun Dis Rep CDR Rev 1996 Feb 02
PMID:An outbreak of Escherichia coli O157 infection linked to paddling pools. 877 43

An outbreak of food poisoning due to Escherichia coli O157 phage type 2 Vero cytotoxin 2 affected 26 people in southern counties of England in May and June 1995. The organism was isolated from faecal specimens from 23 patients, 16 of whom lived in Dorset and seven in Hampshire. Isolates were indistinguishable by phage typing, Vero cytotoxin gene typing, restriction fragment length polymorphism, and pulsed field gel electrophoresis. Three associated cases, linked epidemiologically to the outbreak, were confirmed serologically by detection of antibodies to E. coli O157 lipopolysaccharide. Twenty-two of the 26 patients were adults: four were admitted to hospital with haemorrhagic colitis. Four cases were children: two were admitted to hospital with haemolytic uraemic syndrome (HUS). There were no deaths. Although E. coli O157 was not isolated from any food samples, illness was associated with having eaten cold meats in sandwiches bought from two sandwich producers, in Weymouth and in Portsmouth. Both shops were supplied by the same wholesaler, who kept no records and obtained cooked meats from several sources in packs that did not carry adequate identification marks. It was, therefore, impossible to trace back to the original producer or to investigate further to determine the origin of contamination with E. coli O157. To protect the public health it is essential that all wholesale packs of ready-to-eat food carry date codes and the producer's identification mark. Detailed record keeping should be part of hazard analysis critical control point (HACCP) systems and should be maintained throughout the chain of distribution from the producer to retail outlets.
Commun Dis Rep CDR Rev 1997 Dec 12
PMID:An outbreak of Vero cytotoxin producing Escherichia coli O157 infection associated with takeaway sandwiches. 944 85

In order to explore the structural basis for adaptability in near germline monoclonal antibodies (mAb), we have examined the specificity of the promiscuous mAb S67-27 to both naturally derived carbohydrate antigens and a variety of synthetic nonnatural antigens based on the bacterial lipopolysaccharide component 3-deoxy-alpha-D-manno-oct-2-ulosonic acid (Kdo). One such analog, a 7-O-methyl (7-O-Me) Kdo disaccharide, was found to bind to the antibody with at least 30-fold higher affinity than any other antigen tested. The structure of S67-27 in complex with this analog and three other naturally occurring Kdo antigens revealed that the enhanced affinity of the mAb for the synthetic analog was accomplished by the strategic positioning of CDR H3 away from a conserved Kdo binding pocket that allowed the formation of new antibody-antigen contacts. Furthermore, the comparison of this structure with the structures of related mAbs revealed how the position and structure of CDR H3 influence the specificity or promiscuity of near-germline carbohydrate-recognizing antibodies by altering the architecture of the combining site.
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PMID:The role of CDR H3 in antibody recognition of a synthetic analog of a lipopolysaccharide antigen. 1976 17

Type 1 diabetes is an autoimmune disease mediated by beta cell-specific CD4(+) and CD8(+) T cells. Tracking beta cell-specific T cells is one approach to monitor the diabetogenic response in at risk or diabetic individuals. Such analyses, however, are limited to PBL because T cells infiltrating the pancreatic islets are normally inaccessible. A key issue is whether peripheral beta cell-specific T cells accurately reflect those cells infiltrating the target tissue. We investigated the properties of CD4(+) T cells specific for a mimetic epitope recognized by the BDC2.5 clonotypic TCR in NOD mice. Soluble IA(g7)-Ig (sIA(g7)-Ig) multimer complexes covalently linked to a mimetic BDC peptide (sIA(g7)-mBDC) were used to identify or isolate CD4(+) T cells from PBL and the islets of NOD mice. A temporal increase in sIA(g7)-mBDC binding (g7-mBDC(+)) T cells corresponding with the progression of beta cell autoimmunity was detected in both PBL and islets in NOD female mice. In contrast to T cells in PBL, however, the majority of islet g7-mBDC(+) T cells exhibited a type 1 phenotype, and mediated diabetes upon transfer into NOD.scid recipients. TCR-beta and CDR-beta gene usage of single islet-infiltrating g7-mBDC(+) CD4(+) T cells from individual NOD mice showed a restricted repertoire dominated by one or two clones typically expressing TCR beta-chain variable TRBV-15. In contrast, a distinct and diverse TCR repertoire was detected for PBL-derived g7-mBDC(+) T cells. These results demonstrate that PBL and islet CD4(+) T cells specific for a given beta cell epitope can differ regarding pathogenicity and TCR repertoire.
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PMID:beta cell-specific CD4+ T cell clonotypes in peripheral blood and the pancreatic islets are distinct. 1991 4

The structures of antigen-binding fragments from two related monoclonal antibodies have been determined to high resolution in the presence of several carbohydrate antigens raised against chlamydial lipopolysaccharide. With the exception of CDR H3, antibodies S54-10 and S73-2 are both derived from the same set of germline gene segments as the previously reported structures S25-2 and S45-18. Despite this similarity, the antibodies differ in specificity and the mechanism by which they recognize their cognate antigen. S54-10 uses an unrelated CDR H3 to recognize its antigen in a fashion analogous to S45-18; however, S73-2 recognizes the same antigen as S45-18 and S54-10 in a wholly unrelated manner. Together, these antibody-antigen structures provide snapshots into how the immune system uses the same set of inherited germline gene segments to generate multiple possible specificities that allow for differential recognition of epitopes and how unrelated CDR H3 sequences can result in convergent binding of clinically relevant bacterial antigens.
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PMID:Antibodies raised against chlamydial lipopolysaccharide antigens reveal convergence in germline gene usage and differential epitope recognition. 2000 Jul 57