Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 7 of 7

Publication Record

Connections

Biomimetic glycoliposomes as nanocarriers for targeting P-selectin on activated platelets.
Zhu J, Xue J, Guo Z, Zhang L, Marchant RE
(2007) Bioconjug Chem 18: 1366-9
MeSH Terms: Animals, Binding Sites, Biomimetic Materials, Drug Delivery Systems, Glycolipids, Humans, Hydrophobic and Hydrophilic Interactions, Leukocytes, Lewis Blood Group Antigens, Liposomes, Membrane Glycoproteins, Microscopy, Fluorescence, Nanoparticles, Oligosaccharides, Platelet Activation, Polyethylene Glycols, Vascular Diseases
Show Abstract · Added December 8, 2015
The cell glycocalyx is an attractive model for surface modification of liposomes with the objectives of tissue targeting and prolonged circulation time. Here, we reported on glycocalyx-mimicking liposomes, prepared by incorporating a glycolipid of 3'-sulfo-Lewis a (SuLe(a))-PEG-DSPE with a headgroup of SuLe(a) and a spacer of poly(ethylene glycol) (PEG) linked to two hydrophobic tails. This PEG spaced structure is used to mimic the extended structure of P-selectin glycoprotein ligand 1 (PSGL-1) on activated leukocytes, in order to facilitate the specific binding of liposomes to the receptor of P-selectin expressed on activated platelets. Our results indicate that SuLe(a)-PEG-DSPE can form stable, narrowly distributed liposomes with 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) and cholesterol, with a vesicle size of 113.3 nm. The resultant SuLe(a)-PEG-liposomes can facilitate their binding to the receptor of P-selectin 22 times higher than SuLe(a)-liposomes without a PEG spacer. Further studies by fluorescence microscopy show that SuLe(a)-PEG-liposomes can bind to activated platelets in vitro effectively. It suggests that biomimetic SuLe(a)-PEG-liposomes may be used as nanocarriers to target activated platelets for drug delivery to the injury sites of cardiovascular diseases.
0 Communities
1 Members
0 Resources
17 MeSH Terms
Multiple chromosomal loci for the babA gene in Helicobacter pylori.
Hennig EE, Allen JM, Cover TL
(2006) Infect Immun 74: 3046-51
MeSH Terms: Adhesins, Bacterial, Alleles, Amino Acid Sequence, Base Sequence, Chromosome Mapping, Helicobacter pylori, Lewis Blood Group Antigens, Molecular Sequence Data, Oligosaccharides
Show Abstract · Added March 5, 2014
Helicobacter pylori babA encodes an outer membrane protein that binds to fucosylated Lewis b blood group antigen. We analyzed a panel of 35 H. pylori strains and identified three possible chromosomal loci for babA. There was a significant association between the presence of babA and the presence of cagA (P = 0.0001). Phylogenetic analysis of babA alleles revealed two divergent families of signal sequences. Among 17 strains in which an intact in-frame babA allele was identified, 10 expressed a detectable BabA protein. Expression of a BabA protein and the Lewis b-binding phenotype were not dependent on the chromosomal locus of babA. These data indicate that there is marked heterogeneity among H. pylori strains in babA genetic content and BabA expression.
0 Communities
1 Members
0 Resources
9 MeSH Terms
Heterogeneity among Helicobacter pylori strains in expression of the outer membrane protein BabA.
Hennig EE, Mernaugh R, Edl J, Cao P, Cover TL
(2004) Infect Immun 72: 3429-35
MeSH Terms: Adhesins, Bacterial, Amino Acid Sequence, Carrier Proteins, Genetic Variation, Helicobacter Infections, Helicobacter pylori, Humans, Immunoblotting, Immunoglobulin Variable Region, Lewis Blood Group Antigens, Molecular Sequence Data, Peptide Library, Sequence Alignment, Sequence Analysis, DNA
Show Abstract · Added March 5, 2014
The BabA adhesin of Helicobacter pylori is an outer membrane protein that binds to the fucosylated Lewis b histo-blood group antigen on the surface of gastric epithelial cells. We screened a phage-displayed ScFv (single-chain fragment variable) recombinant antibody library for antibodies reactive with a recombinant BabA fragment and identified two such antibodies. Each antibody recognized an approximately 75-kDa protein present in wild-type H. pylori strain J99 but absent from an isogenic babA mutant strain. An immunoreactive BabA protein was detected by at least one of the antibodies in 18 (46%) of 39 different wild-type H. pylori strains and was detected more commonly in cagA-positive strains than in cagA-negative strains. Numerous amino acid polymorphisms were detected among BabA proteins expressed by different strains, with the greatest diversity occurring in the middle region of the proteins. Among the 18 strains that expressed a detectable BabA protein, there was considerable variation in the level of binding to Lewis b in vitro. Heterogeneity among H. pylori strains in expression of the BabA protein may be a factor that contributes to differing clinical outcomes among H. pylori-infected humans.
0 Communities
1 Members
0 Resources
14 MeSH Terms
Phenotypic diversity in Lewis expression of Helicobacter pylori isolates from the same host.
Wirth HP, Yang M, Peek RM, Höök-Nikanne J, Fried M, Blaser MJ
(1999) J Lab Clin Med 133: 488-500
MeSH Terms: Animals, Antigens, Bacterial, Bacterial Proteins, Female, Gene Expression Regulation, Bacterial, Genotype, Gerbillinae, Helicobacter Infections, Helicobacter pylori, Humans, Lewis Blood Group Antigens, Lewis X Antigen, Male, Mice, Phenotype, Polymerase Chain Reaction, Polymorphism, Genetic, Stomach
Show Abstract · Added March 5, 2014
Populations of Helicobacter pylori cells show a stable expression of Lewis surface antigens, although phase variation may occur among individual organisms grown in vitro. We searched for variation in Lewis phenotypes among H. pylori cells of minimally in vitro-passaged isolates. Lewis expression in 180 clonal H. pylori populations from the primary culture of 20 gastric biopsy samples from 12 patients, and that in 160 isolates from primary cultures from 16 experimentally infected rodents, were examined by enzyme immunoassays. Substantial differences in Lewis expression were found among the isolates from 9 (75%) of 12 patients. These differences were unrelated to overall genetic diversity as determined by polymerase chain reactions for random amplified polymorphic DNA or cagA status, and they persisted during subsequent in vitro passage. In contrast, Lewis expression was highly uniform in H. pylori isolates from different rodents infected for up to 20 weeks. Variation in H. pylori Lewis expression in genetically closely related organisms in human subjects may provide a pool of bacterial phenotypes for the continuous selection of optimally host-adapted populations suitable for persistence.
0 Communities
1 Members
0 Resources
18 MeSH Terms
Acid-induced expression of an LPS-associated gene in Helicobacter pylori.
McGowan CC, Necheva A, Thompson SA, Cover TL, Blaser MJ
(1998) Mol Microbiol 30: 19-31
MeSH Terms: Amino Acid Sequence, Bacterial Proteins, Electrophoresis, Polyacrylamide Gel, Gene Expression Regulation, Bacterial, Genes, Bacterial, Helicobacter pylori, Hydrogen-Ion Concentration, Immunoblotting, Lewis Blood Group Antigens, Lewis X Antigen, Lipopolysaccharides, Molecular Sequence Data, Nucleic Acid Hybridization, O Antigens, Sequence Analysis, DNA
Show Abstract · Added March 5, 2014
To investigate urease-independent mechanisms by which Helicobacter pylori resists acid stress, subtractive RNA hybridization was used to identify H. pylori genes whose expression is induced after exposure to acid pH. This approach led to the isolation of a gene that encoded a predicted 34.8kDa protein (WbcJ), which was homologous to known bacterial O-antigen biosynthesis proteins involved in the conversion of GDP-mannose to GDP-fucose. An isogenic wbcJ null mutant strain failed to express O-antigen and Lewis X or Lewis Y determinants and was more sensitive to acid stress than was the wild-type strain. Qualitative differences in LPS profiles were observed in H. pylori cells grown at pH 5 compared with pH 7, which suggests that H. pylori may alter its LPS structure in response to acidic pH. This may be an important adaptation facilitating H. pylori colonization of the acidic gastric environment.
0 Communities
1 Members
0 Resources
15 MeSH Terms
Ratio of IgG:IgM antibodies to sialyl Lewis(x) and GM3 correlates with tumor growth after immunization with melanoma-cell vaccine with different adjuvants in mice.
Ravindranath MH, Kelley MC, Jones RC, Amiri AA, Bauer PM, Morton DL
(1998) Int J Cancer 75: 117-24
MeSH Terms: Animals, Antibodies, Neoplasm, BCG Vaccine, Cancer Vaccines, Cell Division, Disease Progression, Enzyme-Linked Immunosorbent Assay, G(M3) Ganglioside, Humans, Immunoglobulin G, Immunoglobulin M, Lewis Blood Group Antigens, Lewis X Antigen, Male, Melanoma, Experimental, Mice, Mice, Inbred C57BL
Show Abstract · Added February 16, 2016
Human melanoma cells (from biopsies and culture) express sialyl-Lewis(x) and sialyl Lewis(a), the ligands for ECAM. These ligands may facilitate tumor progression and metastasis in human cancers. To test whether the antibodies to these ligands inhibit tumor progression, IgG and IgM responses to sLe(x) and sLe(a) were induced in C57BL/6j mice (n = 76) by immunization with human melanoma cells, with or without adjuvants (BCG, MPL, KLH). Control mice were treated with saline or BCG. Tumor growth and antigen expression were monitored after challenge with B16 mouse melanoma cells expressing sLe(x), sLe(a) and the ganglioside GM3. Tumor growth was reduced in mice immunized with BCG alone or cells with BCG or MPL, while tumors in mice receiving cells without adjuvants grew larger than in the control. Augmentation of IgM titers to sLe(x) and GM3 after immunization with BCG, or with cells with BCG or MPL correlated with retarded tumor growth, while increased IgG titers to sLe(x) significantly correlated with aggressive tumor growth in mice immunized with cells without adjuvants. SLe(x), sLe(a) and GM3 were expressed in tumors from mice treated with saline or BCG. SLe(x) expression, in particular, was lost in tumors growing in mice immunized with cells with or without adjuvants. Anti-sLe(x) antibodies may promote or prevent tumor growth by antigenic modulation or by cytotoxic killing of tumor cells. Since early anti-sLe(x) IgM correlated with tumor regression, in contrast to anti-sLe(x) IgG, it may serve as a potential early endpoint for the effectiveness of melanoma vaccines expressing the antigens.
0 Communities
1 Members
0 Resources
17 MeSH Terms
Helicobacter pylori Lewis expression is related to the host Lewis phenotype.
Wirth HP, Yang M, Peek RM, Tham KT, Blaser MJ
(1997) Gastroenterology 113: 1091-8
MeSH Terms: Adult, Aged, Aged, 80 and over, Biopsy, Erythrocytes, Female, Gastric Mucosa, Gastritis, Genotype, Helicobacter Infections, Helicobacter pylori, Humans, Inflammation, Lewis Blood Group Antigens, Lewis X Antigen, Male, Middle Aged, Phenotype, Pyloric Antrum
Show Abstract · Added March 5, 2014
BACKGROUND & AIMS - Lewis antigens occur in human gastric epithelium and in Helicobacter pylori lipopolysaccharide; their expression is polymorphic in both. Autoimmune mechanisms induced by bacterial Lewis expression have been proposed to cause gastritis. The aim of this study was to examine the relationship between bacterial and host gastric Lewis expression, as determined by the erythrocyte Lewis(a/b) phenotype, and between gastric histopathology and bacterial Lewis expression.
METHODS - H. pylori Lewis expression was determined by enzyme immunoassays, erythrocyte Lewis phenotype was assessed by agglutination tests, and gastric histopathology was scored blindly.
RESULTS - The host Lewis phenotype was (a+b-) in 15, (a-b+) in 34, and (a-b-) in 17 patients, therefore expressing Lewis x, y, or neither as their major gastric epithelial Lewis type 2 antigen. H. pylori from patients with Lewis(a+b-) expressed Lewis x more than y (1147 +/- 143 vs. 467 +/- 128 optical density units [ODU]; P = 0.006), isolates from patients with Lewis(a-b+) expressed Lewis x less than y (359 +/- 81 vs. 838 +/- 96 ODU; P = 0.0001), and isolates from Lewis(a-b-) patients expressed Lewis x and y approximately equally. Gastritis was unrelated to H. pylori Lewis expression.
CONCLUSIONS - In mimicking host gastric epithelium, H. pylori cells not only express Lewis x and y, but the relative proportion of expression corresponds to the host Lewis phenotype, suggesting selection for host-adapted organisms.
0 Communities
1 Members
0 Resources
19 MeSH Terms