bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of the Antigenic Relationships among Canine Parvovirus Type 2 Variants
Authors: Cavalli Alessandra , Martella Vito , Desario Costantina , Camero Michele , Bellacicco Anna Lucia , De Palo Pasquale , Decaro Nicola , Elia Gabriella , Buonavoglia Canio 
Published: December 2007

ABSTRACT
The antigenic relationships among the original canine parvovirus type 2 (CPV-2) and the variants CPV-2a, -2b, and -2c were evaluated. Cross-antigenic evaluation revealed clear differences among the CPV variants, which were more appreciable by serum neutralization (SN) than by hemagglutination inhibition. Antigenic differences were found mostly between the original CPV-2 and the variants, but they were also observed among the variants CPV-2a, -2b, and -2c. The variant CPV-2c exhibited a unique antigenic pattern, since it was poorly recognized by the sera of animals immunized with CPV-2, CPV-2a, and CPV-2b. However, animals immunized with CPV-2c exhibited higher SN titers to CPV-2b than to the homologous virus CPV-2c. The observed antigenic differences might drive selection of CPV strains by generating differential immune pressure in the canine population, which raises concerns about vaccine efficacy.
Class II-Restricted Protective Immunity Induced by Malaria Sporozoites
Authors: Oliveira Giane A. , Kumar Kota Arun , Calvo-Calle J. Mauricio , Othoro Caroline , Altszuler David , Nussenzweig Victor , Nardin Elizabeth H. 
Published: December 2007

ABSTRACTThe irradiated-sporozoite vaccine elicits sterile immunity againstPlasmodiumparasites in experimental rodent hosts and human volunteers. Based on rodent malaria models, it has been proposed that CD8+T cells are the key protective effector mechanism required in sporozoite-induced immunity. To investigate the role of class II-restricted immunity in protective immunity, we immunized β2-microglobulin knockout (β2M−/−) mice with irradiatedPlasmodium yoeliiorP. bergheisporozoites. Sterile immunity was obtained in the CD8+-T-cell-deficient mice immunized with eitherP. bergheiorP. yoeliisporozoites. β2M−/−mice with the BALB/c (H-2d) genetic background as well as those with the C57BL (H-2b) genetic background were protected. Effector mechanisms included CD4+T cells, mediated in part through the production of gamma interferon, and neutralizing antibodies that targeted the extracellular sporozoites. We conclude that in the absence of class I-restricted CD8+T cells, sporozoite-induced protective immunity can be effectively mediated by class II-restricted immune effector mechanisms. These results support efforts to develop subunit vaccines that effectively elicit high levels of antibody and CD4+T cells to targetPlasmodiumpreerythrocytic stages.
Peritoneal Challenge Modulates Expression of Pneumococcal Surface Protein C during Bacteremia in Mice
Authors: Quin Lisa R. , Moore Quincy C. , Thornton Justin A. , McDaniel Larry S. 
Published: December 2007

ABSTRACT

Differential expression of pneumococcal virulence proteins has been demonstrated. We previously demonstrated challenge route-dependent differences in pneumococcal surface protein C (PspC) expression during bacteremia. In this study, we investigated differences in PspC expression during the transition of pneumococci from the peritoneum to the blood. Time course analysis of PspC expression using flow cytometry demonstrated that
Streptococcus pneumoniae
D39 collected from blood expressed significantly more PspC than did D39 collected from the peritoneum of intraperitoneally (i.p.)-infected mice. Various challenge models were then used to determine whether host responses originating from the peritoneum can influence PspC expressed by pneumococci in the blood. Using heat-inactivated D39 (HI-D39) and sterile peritoneal dialysis fluid (PDF), we investigated whether stimulation of peritoneal responses can influence PspC expression. Injection of mice i.p. with HI-D39 or PDF immediately prior to intravenous (i.v.) infection with D39 caused a significant increase in PspC expressed by D39 in the blood. Finally, we used cytokine array analysis to investigate specific inflammatory mediators that may result in differential PspC expression. Of the 96 inflammatory cytokines assayed, D39 i.p. challenge led to increased expression of 33 cytokines in serum; whereas D39 i.v. challenge led to increased expression of 15 and decreased expression of 11 cytokines relative to serum of the uninfected control. These results indicate that PspC is differentially regulated during growth in vivo and that the level of expression varies depending on the host environment.
The Proteasome Immunosubunit Multicatalytic Endopeptidase Complex-Like 1 Is a T-Cell-Intrinsic Factor Influencing Homeostatic Expansion
Authors: Zaiss Dietmar M. W. , de Graaf Natascha , Sijts Alice J. A. M. 
Published: December 2007

ABSTRACT

Homeostatic regulatory mechanisms maintain the constant ratios between different lymphocyte subsets in the secondary lymphoid organs. How this dynamic equilibrium is achieved, in particular following the clonal expansion and subsequent contraction of different cells after infection, remains poorly understood. Expression of the proteasome immunosubunits has been shown to influence not only major histocompatibility complex class I (MHC-I) antigen processing and thereby T-cell responses, but also the CD4/CD8 T-cell ratios in lymphoid organs. We examined the relationships between these different immunosubunit-mediated effects in mice of various proteasome subunit compositions during infection with
Listeria monocytogenes
. Mice that lacked the immunosubunit multicatalytic endopeptidase complex-like 1 (MECL-1) maintained enhanced CD4/CD8 T-cell ratios during infection, while MHC-I surface levels resembled those in wild-type (wt) mice. LMP7 gene-deficient mice, on the other hand, showed reduced MHC-I expression, while their splenic CD4/CD8 ratios were similar to those in wt mice. Remarkably, analysis of bone marrow-chimeric immunosubunit gene-deficient mice, reconstituted with a mixture of wt and LMP7- plus MECL-1-deficient bone marrow, revealed that the LMP7- plus MECL-1-deficient T-cell population maintained a higher CD4/CD8 T-cell ratio than the wt T-cell population before, during, and after infection and T-cell memory formation. Since in these mice the immunosubunit-positive and immunosubunit-negative T-cell populations were selected in the same thymus and expanded in the same lymphoid environments, our findings indicate that MECL-1 influences the homeostatic equilibrium between T-cell subsets, not through indirect extracellular signals, such as MHC-I expression or the cytokine milieu, but through direct effects on T-cell-intrinsic processes.
Expression of Cathelicidin LL-37 duringMycobacterium tuberculosisInfection in Human Alveolar Macrophages, Monocytes, Neutrophils, and Epithelial Cells
Authors: Rivas-Santiago Bruno , Hernandez-Pando Rogelio , Carranza Claudia , Juarez Esmeralda , Contreras Juan Leon , Aguilar-Leon Diana , Torres Martha , Sada Eduardo 
Published: December 2007

ABSTRACTThe innate immune response in human tuberculosis is not completely understood. To improve our knowledge regarding the role of cathelicidin hCAP-18/LL37 in the innate immune response to tuberculosis infection, we used immunohistochemistry, immunoelectron microscopy, and gene expression to study the induction and production of the antimicrobial peptide in A549 epithelial cells, alveolar macrophages (AM), neutrophils, and monocyte-derived macrophages (MDM) after infection withMycobacterium tuberculosis. We demonstrated that mycobacterial infection induced the expression and production of LL-37 in all cells studied, with AM being the most efficient. We did not detect peptide expression in tuberculous granulomas, suggesting that LL-37 participates only during early infection. Through the study of Toll-like receptors (TLR) in MDM, we showed that LL-37 can be induced by stimulation through TLR-2, TLR-4, and TLR-9. This last TLR was strongly stimulated byM. tuberculosisDNA. We concluded that LL-37 may have an important role in the innate immune response againstM. tuberculosis.
Coordinate Regulation of
Salmonella
Pathogenicity Island 1 (SPI1) and SPI4 in
Salmonella enterica
Serovar Typhimurium
Authors: Main-Hester Kara L. , Colpitts Katherine M. , Thomas Gracie A. , Fang Ferric C. , Libby Stephen J. 
Published: December 2007

ABSTRACT

Salmonella enterica
serovar Typhimurium harbors five pathogenicity islands (SPI) required for infection in vertebrate hosts. Although the role of SPI1 in promoting epithelial invasion and proinflammatory cell death has been amply documented, SPI4 has only more recently been implicated in
Salmonella
virulence. SPI4 is a 24-kb pathogenicity island containing six open reading frames,
siiA
to
siiF
. Secretion of the 595-kDa SiiE protein requires a type I secretory system encoded by
siiC
,
siiD
, and
siiF
. An operon polarity suppressor (
ops
) sequence within the 5′ untranslated region upstream of
siiA
is required for optimal SPI4 expression and predicted to bind the antiterminator RfaH. SiiE concentrations are decreased in a SPI1 mutant strain, suggesting that SPI1 and SPI4 may have common regulatory inputs. SPI1 gene expression is positively regulated by the transcriptional activators HilA, HilC, and HilD, encoded within SPI1, and negatively regulated by the regulators HilE and PhoP. Here, we show that mutations in
hilA
,
hilC
, or
hilD
similarly reduce expression of
siiE
, and mutations in
hilE
or
phoP
enhance
siiE
expression. Individual overexpression of HilA, HilC, or HilD in the absence of SPI1 cannot activate
siiE
expression, suggesting that these transcriptional regulators act in concert or in combination with additional SPI1-encoded regulatory loci to activate SPI4. HilA is no longer required for
siiE
expression in an
hns
mutant strain, suggesting that HilA promotes SPI4 expression by antagonizing the global transcriptional silencer H-NS. Coordinate regulation suggests that SPI1 and SPI4 play complementary roles in the interaction of
S. enterica
serovar Typhimurium with the host intestinal mucosa.
The Hek Outer Membrane Protein of
Escherichia coli
Strain RS218 Binds to Proteoglycan and Utilizes a Single Extracellular Loop for Adherence, Invasion, and Autoaggregation
Authors: Fagan Robert P. , Lambert Matthew A. , Smith Stephen G. J. 
Published: December 2007

ABSTRACT

Escherichia coli
is the principal gram-negative causative agent of sepsis and meningitis in neonates. The pathogenesis of meningitis due to
E. coli
K1 involves mucosal colonization, transcytosis of epithelial cells, survival in the bloodstream, and eventually invasion of the meninges. The last two aspects have been well characterized at a molecular level. Less is known about the early stages of pathogenesis, i.e., adhesion to and invasion of epithelial cells. We have previously reported that the Hek protein causes autoaggregation and can mediate adherence to and invasion of epithelial cells. Here, we report that Hek-mediated adherence is dependent on binding to glycosoaminoglycan, in particular, heparin. The ability to hemagglutinate, autoaggregate, adhere, and invade is contingent on a putative 25-amino-acid loop that is exposed to the outside of the bacterial cells.
C-Terminal Repeats ofClostridium difficileToxin A Induce Production of Chemokine and Adhesion Molecules in Endothelial Cells and Promote Migration of Leukocytes
Authors: Yeh Chiou-Yueh , Lin Chun-Nan , Chang Chuan-Fa , Lin Chun-Hung , Lien Huei-Ting , Chen Jen-Yang , Chia Jean-San 
Published: December 2007

ABSTRACTThe C-terminal repeating sequences ofClostridium difficiletoxin A (designated ARU) are homologous to the carbohydrate-binding domain of streptococcal glucosyltransferases (GTFs) that were recently identified as potent modulins. To test the hypothesis that ARU might exert a similar biological activity on endothelial cells, recombinant ARU (rARU), which was noncytotoxic to cell cultures, was analyzed using human umbilical vein endothelial cells. The rARU could bind directly to endothelial cells in a serum- and calcium-dependent manner and induce the production of interleukin-6 (IL-6), IL-8, and monocyte chemoattractant protein 1 in a dose-dependent manner. An oligosaccharide binding assay indicated that rARU, but not GTFC, binds preferentially to Lewis antigens and 3′HSO3-containing oligosaccharides. Binding of rARU to human endothelial or intestinal cells correlated directly with the expression of Lewis Y antigen. Bound rARU directly activated mitogen-activated protein kinases and the NF-κB signaling pathway in endothelial cells to release biologically active chemokines and adhesion molecules that promoted migration in a transwell assay and the adherence of polymorphonuclear and mononuclear cells to the endothelial cells. These results suggest that ARU may bind to multiple carbohydrate motifs to exert its biological activity on human endothelial cells.
Differential Uptake and Processing of a
Haemophilus influenzae
P5-Derived Immunogen by Chinchilla Dendritic Cells
Authors: Novotny Laura A. , Partida-Sánchez Santiago , Munson Robert S. , Bakaletz Lauren O. 
Published: December 2007

ABSTRACT

Dendritic cells (DCs) are potent antigen-presenting cells involved in the initiation and modulation of immune responses after immunization via their ability to process and present antigen to naive T cells. We wanted to examine the role of DCs in the development of protective immunity against nontypeable
Haemophilus influenzae
(NTHI)-induced experimental otitis media (OM) after intranasal immunization of chinchillas with an NTHI P5-derived synthetic peptide immunogen called LB1. As chinchilla DCs have not been described, we adapted well-established protocols to induce the differentiation of chinchilla bone marrow precursor cells into DCs, which resulted in cells that were morphologically and phenotypically similar to DCs of other species. In vitro, chinchilla DCs readily internalized LB1, upregulated expression of the maturation markers CD80 and major histocompatibility complex class II, and presented processed LB1 to primed CD3
+
T cells, which resulted in antigen-specific T-cell proliferation. In vivo, LB1-activated DCs trafficked from the chinchilla nasal cavity primarily to the nasal-associated lymphoid tissues and were detected in close proximity to CD3
+
T cells within this lymphoid aggregate. These data are the first to characterize chinchilla DCs and their functional properties. Furthermore, they suggest an important role for chinchilla DCs in the development of protective immunity against experimental NTHI-induced OM after intranasal immunization.
Enteric Salmonellosis Disrupts the Microbial Ecology of the Murine Gastrointestinal Tract
Authors: Barman Melissa , Unold David , Shifley Kathleen , Amir Elad , Hung Kueichun , Bos Nicolaas , Salzman Nita 
Published: December 2007

ABSTRACT

The commensal microbiota protects the murine host from enteric pathogens. Nevertheless, specific pathogens are able to colonize the intestinal tract and invade, despite the presence of an intact biota. Possibly, effective pathogens disrupt the indigenous microbiota, either directly through pathogen-commensal interaction, indirectly via the host mucosal immune response to the pathogen, or by a combination of these factors. This study investigates the effect of peroral
Salmonella enterica
serovar Typhimurium infection on the intestinal microbiota. Since the majority of the intestinal microbiota cannot be cultured by conventional techniques, molecular approaches using 16S rRNA sequences were applied. Several major bacterial groups were assayed using quantitative PCR. Administration of either the 50% lethal dose (LD
50
) or 10× LD
50
of
Salmonella enterica
serovar Typhimurium caused changes in the microbiota throughout the intestinal tract over the time course of infection. A 95% decrease in total bacterial number was noted in the cecum and large intestine with 10× LD
50
S. enterica
serovar Typhimurium challenge at 7 days postinfection, concurrent with gross evidence of diarrhea. In addition, alterations in microbiota composition preceded the onset of diarrhea, suggesting the involvement of pathogen-commensal interactions and/or host responses unrelated to diarrhea. Microbiota alterations were not permanent and reverted to the microbiota of uninfected mice by 1 month postinfection. Infection with a
Salmonella
pathogenicity island 1 (SPI1) mutant did not result in microbiota alterations, while SPI2 mutant infections triggered partial changes. Neither mutant was capable of prolonged colonization or induction of mucosal inflammation. These data suggest that several
Salmonella
virulence factors, particularly those involved in the local mucosal host response, are required for disruption of the intestinal ecosystem.
DNA Microarray Based on Arrayed-Primer Extension Technique for Identification of Pathogenic Fungi Responsible for Invasive and Superficial Mycoses
Authors: Campa Daniele , Tavanti Arianna , Gemignani Federica , Mogavero Crocifissa S. , Bellini Ilaria , Bottari Fabio , Barale Roberto , Landi Stefano , Senesi Sonia 
Published: December 2007

ABSTRACT

An oligonucleotide microarray based on the arrayed-primer extension (APEX) technique has been developed to simultaneously identify pathogenic fungi frequently isolated from invasive and superficial infections. Species-specific oligonucleotide probes complementary to the internal transcribed spacer 1 and 2 (ITS1 and ITS2) region were designed for 24 species belonging to 10 genera, including
Candida
species (
Candida albicans
,
Candida dubliniensis
,
Candida famata
,
Candida glabrata
,
Candida tropicalis
,
Candida kefyr
,
Candida krusei
,
Candida guilliermondii
,
Candida lusitaniae
,
Candida metapsilosis
,
Candida orthopsilosis
,
Candida parapsilosis
, and
Candida pulcherrima
),
Cryptococcus neoformans
,
Aspergillus
species (
Aspergillus fumigatus
and
Aspergillus terreus
),
Trichophyton
species (
Trichophyton rubrum
and
Trichophyton tonsurans
),
Trichosporon cutaneum
,
Epidermophyton floccosum
,
Fusarium solani
,
Microsporum canis
,
Penicillium marneffei
, and
Saccharomyces cerevisiae
. The microarray was tested for its specificity with a panel of reference and blinded clinical isolates. The APEX technique was proven to be highly discriminative, leading to unequivocal identification of each species, including the highly related ones
C. parapsilosis
,
C. orthopsilosis
, and
C. metapsilosis
. Because of the satisfactory basic performance traits obtained, such as reproducibility, specificity, and unambiguous interpretation of the results, this new system represents a reliable method of potential use in clinical laboratories for parallel one-shot detection and identification of the most common pathogenic fungi.
Determination of Accessory Gene Patterns Predicts the Same Relatedness among Strains of
Streptococcus pneumoniae
as Sequencing of Housekeeping Genes Does and Represents a Novel Approach in Molecular Epidemiology
Authors: Dagerhamn Jessica , Blomberg Christel , Browall Sarah , Sjöström Karin , Morfeldt Eva , Henriques-Normark Birgitta 
Published: December 2007

ABSTRACT

Relatedness between isolates of
Streptococcus pneumoniae
can be determined from sequences of multiple genes belonging to the core genome (multilocus sequence typing [MLST]), but these do not provide information on gene content that may affect the potential of isolates to cause invasive pneumococcal disease. Gene content data, obtained using microarrays, were gathered for 40 clinical isolates of 12 serotypes belonging to 30 multilocus sequence types. We found that sequence variations in housekeeping genes assessed by MLST correlated well with whole-genome microarray analyses identifying the presence/absence of accessory genes/regions. However, isolates belonging to the same clonal complex, as determined by MLST, may not have identical gene contents, potentially affecting virulence. We found fewer intraclonal (same MLST sequence type) differences associated with pneumococcal serotypes of high invasive disease potential, i.e., serotypes rarely found among carriers compared to serotypes frequently found in carriage. Molecular typing of pneumococci based on the presence/absence of 25 genes localized to accessory regions shows the same relatedness among pneumococcal strains as MLST does. We conclude that molecular typing of pneumococci based on variation in the nucleotide sequences of parts of housekeeping genes (MLST) correlates with the presence/absence of genes in the accessory part of the genome. This covariation is likely due to the fact that both sequence variations and gene content variations are created primarily by recombination events in pneumococci.
Identification of Clinical Coryneform Bacterial Isolates: Comparison of Biochemical Methods and Sequence Analysis of 16S rRNA and
rpoB
Genes
Authors: Adderson Elisabeth E. , Boudreaux Jan W. , Cummings Jessica R. , Pounds Stanley , Wilson Deborah A. , Procop Gary W. , Hayden Randall T. 
Published: December 2007

ABSTRACT

We compared the relative levels of effectiveness of three commercial identification kits and three nucleic acid amplification tests for the identification of coryneform bacteria by testing 50 diverse isolates, including 12 well-characterized control strains and 38 organisms obtained from pediatric oncology patients at our institution. Between 33.3 and 75.0% of control strains were correctly identified to the species level by phenotypic systems or nucleic acid amplification assays. The most sensitive tests were the API Coryne system and amplification and sequencing of the 16S rRNA gene using primers optimized for coryneform bacteria, which correctly identified 9 of 12 control isolates to the species level, and all strains with a high-confidence call were correctly identified. Organisms not correctly identified were species not included in the test kit databases or not producing a pattern of reactions included in kit databases or which could not be differentiated among several genospecies based on reaction patterns. Nucleic acid amplification assays had limited abilities to identify some bacteria to the species level, and comparison of sequence homologies was complicated by the inclusion of allele sequences obtained from uncultivated and uncharacterized strains in databases. The utility of
rpoB
genotyping was limited by the small number of representative gene sequences that are currently available for comparison. The correlation between identifications produced by different classification systems was poor, particularly for clinical isolates.