bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunization with cDNA Expressed by Amastigotes ofTrypanosoma cruziElicits Protective Immune Response against Experimental Infection
Authors: Boscardin Silvia B. , Kinoshita Sheila S. , Fujimura Adriana E. , Rodrigues Mauricio M. 
Published: April 2003

ABSTRACTImmunization of mice with plasmids containingTrypanosoma cruzigenes induced specific antibodies, CD4+Th1 and CD8+Tc1 cells, and protective immunity against infection. In most cases, plasmids used for DNA vaccination contained genes encoding antigens expressed by trypomastigotes, the nonreplicative forms of the parasite. In this study, we explored the possibility of using genes expressed by amastigotes, the form of the parasite which replicates inside host cells, for experimental DNA vaccination. For that purpose, we selected a gene related to the amastigote surface protein 2 (ASP-2), an antigen recognized by antibodies and T cells from infected mice and humans, for our study. Using primers specific for theasp-2gene, four distinct groups of genes were amplified from cDNA from amastigotes of the Y strain ofT. cruzi. At the nucleotide level, they shared 82.3 to 89.9% identity with the previously describedasp-2gene. A gene namedclone 9presented the highest degree of identity with theasp-2gene and was selected for immunological studies. Polyclonal antisera raised against the C terminus of the recombinant protein expressed by theclone 9gene reacted with an antigen of approximately 83 kDa expressed in amastigotes ofT. cruzi. Immunization of BALB/c mice with eukaryotic expression plasmids containing theclone 9gene elicited specific antibodies and CD4+T-cell-dependent gamma interferon secretion. Upon challenge with trypomastigotes, mice immunized with plasmids harboring theclone 9gene displayed reduced parasitemia and survived lethal infection. We concluded that amastigote cDNA is an interesting source of antigens that can be used for immunological studies, as well as for vaccine development.
Inhibition of Gamma Interferon Decreases Bacterial Load in Peritonitis by Accelerating Peritoneal Fibrin Deposition and Tissue Repair
Authors: Qiu Gang , Gribbin Elizabeth , Harrison Kathryn , Sinha Neil , Yin Kingsley 
Published: April 2003

ABSTRACTBowel perforation can lead to significant bacterial spillage, which may then cause septic peritonitis, characterized by a systemic inflammatory response and organ dysfunction. There are several reports that have shown that the development of peritoneal adhesions is dependent on inflammatory cytokine levels and that these adhesions can reduce bacterial spread, possibly by sealing off the cecum in the cecal ligation and puncture (CLP) model of septic peritonitis. There have not, however, been any studies that have utilized a strategy to accelerate tissue repair in order to seal off the injured cecum and reduce bacterial spread as well as ameliorate systemic inflammation. In the present study, we demonstrate that the administration of anti-gamma interferon (IFN-γ) antibody (1.2 mg/kg of body weight, intravenously) accelerated tissue repair via increased fibrin deposition 12 and 24 h after CLP in rats. This increase in fibrin deposition was associated with peritoneal adhesion 24 h after CLP and a reduction in bacterial load compared to the bacterial load of rats given irrelevant antibody. Plasma fibrin levels, however, were not altered after IFN-γ antibody administration, suggesting that the inhibition of IFN-γ activity specifically increased fibrin deposition to the site of injury. Furthermore, plasma interleukin-6, used as a marker of systemic inflammatory response, was reduced in CLP rats given IFN-γ antibody compared to that found in those given irrelevant antibody. These results suggest that the early inhibition of IFN-γ activity in the CLP model is beneficial by accelerating fibrin deposition in cecal tissue to prevent bacterial spread and reduce the systemic inflammatory response. Importantly, increased fibrin deposition in the ceca was not associated with increased plasma fibrin whereas the latter may have detrimental effects associated with coagulation disorders.
Complete Genome Sequence and Comparative Genomics ofShigella flexneriSerotype 2a Strain 2457T
Authors: Wei J. , Goldberg M. B. , Burland V. , Venkatesan M. M. , Deng W. , Fournier G. , Mayhew G. F. , Plunkett G. , Rose D. J. , Darling A. , Mau B. , Perna N. T. , Payne S. M. , Runyen-Janecky L. J. , Zhou S. , Schwartz D. C. , Blattner F. R. 
Published: April 2003

ABSTRACTWe determined the complete genome sequence ofShigella flexneriserotype 2a strain 2457T (4,599,354 bp).Shigellaspecies cause >1 million deaths per year from dysentery and diarrhea and have a lifestyle that is markedly different from those of closely related bacteria, includingEscherichia coli. The genome exhibits the backbone and island mosaic structure ofE. colipathogens, albeit with much less horizontally transferred DNA and lacking 357 genes present inE. coli. The strain is distinctive in its large complement of insertion sequences, with several genomic rearrangements mediated by insertion sequences, 12 cryptic prophages, 372 pseudogenes, and 195S. flexneri-specific genes. The 2457T genome was also compared with that of a recently sequencedS. flexneri2a strain, 301. Our data are consistent withShigellabeing phylogenetically indistinguishable fromE. coli. TheS. flexneri-specific regions contain many genes that could encode proteins with roles in virulence. Analysis of these will reveal the genetic basis for aspects of this pathogenic organism's distinctive lifestyle that have yet to be explained.
Role of Surface-Exposed Loops ofHaemophilus influenzaeProtein P2 in the Mitogen-Activated Protein Kinase Cascade
Authors: Galdiero Stefania , Capasso Domenica , Vitiello Mariateresa , D'Isanto Marina , Pedone Carlo , Galdiero Massimiliano 
Published: April 2003

ABSTRACTThe outer membrane of gram-negative bacteria contains several proteins, and some of these proteins, the porins, have numerous biological functions in the interaction with the host; porins are involved in the activation of signal transduction pathways and, in particular, in the activation of the Raf/MEK1-MEK2/mitogen-activated protein kinase (MAPK) cascade. The P2 porin is the most abundant outer membrane protein ofHaemophilus influenzaetype b. A three-dimensional structural model for P2 was constructed based on the crystal structures ofKlebsiella pneumoniaeOmpK36 andEscherichia coliPhoE and OmpF. The protein was readily assembled into the β-barrel fold characteristic of porins, despite the low sequence identity with the template proteins. The model provides information on the structural features of P2 and insights relevant for prediction of domains corresponding to surface-exposed loops, which could be involved in the activation of signal transduction pathways. To identify the role of surface-exposed loops, a set of synthetic peptides were synthesized according to the proposed model and were assayed for MEK1-MEK2/MAPK pathway activation. Our results show that synthetic peptides corresponding to surface loops of protein P2 are able to activate the MEK1-MEK2/MAPK pathways like the entire protein, while peptides modeled on internal β strands are unable to induce significant phosphorylation of the MEK1-MEK2/MAPK pathways. In particular, the peptides corresponding to loops L5 (Lys206 to Gly219), L6B (Ser239 to Lys253), and L7 (Thr280 to Lys287) activate, as the whole protein, essentially JNK and p38.
Genome Diversification in
Staphylococcus aureus
: Molecular Evolution of a Highly Variable Chromosomal Region Encoding the Staphylococcal Exotoxin-Like Family of Proteins
Authors: Fitzgerald J. Ross , Reid Sean D. , Ruotsalainen Eeva , Tripp Timothy J. , Liu MengYao , Cole Robert , Kuusela Pentti , Schlievert Patrick M. , Järvinen Asko , Musser James M. 
Published: April 2003

ABSTRACT

Recent genomic studies have revealed extensive variation in natural populations of many pathogenic bacteria. However, the evolutionary processes which contribute to much of this variation remain unclear. A previous whole-genome DNA microarray study identified variation at a large chromosomal region (RD13) of
Staphylococcus aureus
which encodes a family of proteins with homology to staphylococcal and streptococcal superantigens, designated staphylococcal exotoxin-like (SET) proteins. In the present study, RD13 was found in all 63
S. aureus
isolates of divergent clonal, geographic, and disease origins but contained a high level of variation in gene content in different strains. A central variable region which contained from 6 to 10 different
set
genes, depending on the strain, was identified, and DNA sequence analysis suggests that horizontal gene transfer and recombination have contributed to the diversification of RD13. Phylogenetic analysis based on the RD13 DNA sequence of 18 strains suggested that loss of various
set
genes has occurred independently several times, in separate lineages of pathogenic
S. aureus
, providing a model to explain the molecular variation of RD13 in extant strains. In spite of multiple episodes of
set
deletion, analysis of the ratio of silent substitutions in
set
genes to amino acid replacements in their products suggests that purifying selection (selective constraint) is acting to maintain SET function. Further, concurrent transcription in vitro of six of the seven
set
genes in strain COL was detected, indicating that the expression of
set
genes has been maintained in contemporary strains, and Western immunoblot analysis indicated that multiple SET proteins are expressed during the course of human infections. Overall, we have shown that the chromosomal region RD13 has diversified extensively through episodes of gene deletion and recombination. The coexpression of many
set
genes and the production of multiple SET proteins during human infection suggests an important role in host-pathogen interactions.
Coordinate Regulation ofSalmonella entericaSerovar Typhimurium Invasion of Epithelial Cells by the Arp2/3 Complex and Rho GTPases
Authors: Criss Alison K. , Casanova James E. 
Published: April 2003

ABSTRACTSalmonella entericaserovar Typhimurium can infect epithelial cells via the basolateral surface after breaching the intestinal epithelium, yet little is known about this process. Here, we show that actin polymerization driven by the Arp2/3 complex is critical to both basolateral and apical bacterial invasion of polarized MDCK cells. While there is also a dependence upon toxin B-sensitive Rho GTPases, none of the four GTPases known to be activated byS. entericaserovar Typhimurium SopE are individually required for basolateral internalization. These results underscore that the specific factors required forSalmonellainvasion differ between membrane domains of polarized epithelia.
Expression of a
luxS
Gene Is Not Required for
Borrelia burgdorferi
Infection of Mice via Needle Inoculation
Authors: Hübner Anette , Revel Andrew T. , Nolen Dena M. , Hagman Kayla E. , Norgard Michael V. 
Published: April 2003

ABSTRACT

The
luxS
gene product is an integral component of LuxS/autoinducer-2 (AI-2) quorum-sensing systems in bacteria. A putative
luxS
gene was expressed at comparable levels by
Borrelia burgdorferi
strain 297 cultivated either in vitro or in dialysis membrane chambers implanted in rat peritoneal cavities. Although the borrelial
luxS
gene functionally complemented a LuxS deficiency in
Escherichia coli
DH5α, AI-2-like activity could not be detected within
B. burgdorferi
culture supernatants or concentrated cell lysates. Finally, a
luxS
-deficient mutant of
B. burgdorferi
was infectious at wild-type levels when it was intradermally needle inoculated into mice, indicating that expression of
luxS
probably is not required for infectivity but, at the very least, is not essential for mammalian host adaptation. Our findings also challenge the notion that a LuxS/AI-2 quorum-sensing system is operative in
B. burgdorferi
.
Molecular Patchwork: Chromosomal Recombination between Two
Helicobacter pylori
Strains during Natural Colonization
Authors: Smeets Leonard C. , Arents Nicolaas L. A. , van Zwet Anton A. , Vandenbroucke-Grauls Christina M. J. E. , Verboom Theo , Bitter Wilbert , Kusters Johannes G. 
Published: April 2003

ABSTRACT

Genetic analysis of two
Helicobacter pylori
strains isolated from a single gastric biopsy showed evidence of extensive horizontal gene transfer. Several large recombinations were identified in the
rdxA
gene, which is involved in metronidazole resistance.
fhuAofActinobacillus pleuropneumoniaeEncodes a Ferrichrome Receptor but Is Not Regulated by Iron
Authors: Mikael Leonie G. , Srikumar Ramakrishnan , Coulton James W. , Jacques Mario 
Published: April 2003

ABSTRACTThe swine pathogenActinobacillus pleuropneumoniaepossesses a 75-kDa outer membrane protein (OMP), FhuA, the receptor for ferrichrome, a hydroxamate-type siderophore. Polyclonal serum to FhuA reacted with OMP preparations from 12 serotypes ofA. pleuropneumoniaeunder conditions of iron repletion and restriction. Reverse transcription-PCR confirmed thatA. pleuropneumoniae fhuAexpression is not upregulated in response to low iron levels. AnA. pleuropneumoniae fhuAdeletion mutant was generated and showed abolishment of ferrichrome uptake.
Th1 Cell Development Induced by Cysteine Proteinases A and B in Localized Cutaneous Leishmaniasis Due to
Leishmania guyanensis
Authors: Pascalis Hervé , Lavergne Anne , Bourreau Eliane , Prévot-Linguet Ghislaine , Kariminia Amina , Pradinaud Roger , Rafati Sima , Launois Pascal 
Published: April 2003

ABSTRACT

The cysteine proteinases CPA and CPB from
Leishmania major
induced Th1 responses in patients with leishmaniasis due to
Leishmania guyanensis
. Furthermore, cysteine proteinases induced neither interleukin 4 (IL-4) nor IL-13 and low levels of IL-10 in controls and patients. The results suggest that CPs would be quite good candidates for a vaccine against different
Leishmania
species.
Vγ9Vδ2 T-Cell Anergy and Complementarity-Determining Region 3-Specific Depletion during Paroxysm of Nonendemic Malaria Infection
Authors: Martini Federico , Paglia Maria Grazia , Montesano Carla , Enders Patrick J. , Gentile Marco , Pauza C. David , Gioia Cristiana , Colizzi Vittorio , Narciso Pasquale , Pucillo Leopoldo Paolo , Poccia Fabrizio 
Published: April 2003

ABSTRACTVγ9Vδ2 T lymphocytes strongly respond to phosphoantigens fromPlasmodiumparasites. Thus, we analyzed the changes in Vγ9Vδ2 T-cell function and repertoire during the paroxysm phase of nonendemic malaria infection. During malaria paroxysm, Vγ9Vδ2 T cells were early activated but rapidly became anergic and finally loose Jγ1.2 Vγ9 complementarity-determining region 3 transcripts.
Binding of Intimin from EnteropathogenicEscherichia colito Lymphocytes and Its Functional Consequences
Authors: Gonçalves Nathalie S. , Hale Christine , Dougan Gordon , Frankel Gad , MacDonald Thomas T. 
Published: April 2003

ABSTRACTIntimin-conjugated fluorescent beads bind to spleen CD4 T cells and Peyer's patch, mesenteric lymph node, and cecal follicle lymphocytes, with less binding to lamina propria T cells and intraepithelial lymphocytes. Intimin costimulates proliferation of spleen CD4 T cells and cells from organized lymphoid tissues but does not costimulate cells from the lamina propria of normal or inflamed colon.
Unresponsiveness to Surface Antigen 1 Modifies Cytokine Profiles in Acute <i>Toxoplasma gondii</i> Infection
Authors: Seng S. , Makala L.H.C. , Maki Y. , Choi Y. , Yokoyama M. , Suzuki N. , Toyoda Y. , Nagasawa H. 
Published: April 2003

Resistance to <i>Toxoplasma gondii</i> involves the development of a highly polarized Th1-type cytokine expression. <i>SAG1</i> transgenic mice are highly susceptible to <i>T. gondii</i> infection due to their non-reactivity to SAG1 of the protozoan parasite. Here we describe cytokine profiles during the acute phase of <i>T. gondii</i> infection, which are associated with the susceptibility of <i>SAG1</i> transgenic mice. <i>SAG1</i> transgenic mice showed a 4.5-fold increase in susceptibility upon inoculation with a sublethal dose of the Beverley strain of <i>T. gondii</i> compared to their wild-type counterparts (mortality: 81 vs. 18%, respectively). When analysis of the most important cytokines involved in the mediation of resistance to infection was carried out, <i>SAG1</i> transgenic mice exhibited low production levels of IL-12, IFN-γ and TNF-α in sera during the acute phase of <i>T. gondii</i> infection. Antibody and T cells specific for SAG1 were not mounted upon SAG1 stimulation in <i>SAG1</i> transgenic mice. Moreover, in vitro studies indicated that in <i>SAG1</i> transgenic mice IFN-γ and IL-12 production was lower than in their wild-type counterparts, although levels of TNF-α increased in <i>SAG1</i> transgenic mice on day 9 after infection. Low IgG2a levels were detected in <i>SAG1</i> transgenic mouse sera. Unresponsiveness to SAG1 of <i>T. gondii</i> renders <i>SAG1</i> transgenic mice unable to develop a strong Th1-based protection against <i>T. gondii</i> infection. These results provide evidence that SAG1 is a pivotal antigen involved in the induction of immune responses towards the development of Th1-protective immunity during <i>T. gondii</i> infection.
A FRESH LOOK AT MALACHI II 13-16
Authors: Zehnder Markus 
Published: April 2003

AbstractIn this study it is argued that the main thrust of Mal. ii 13-16 is against those men within the YHWH-congregation in Yehud, who expel their first, "Israelite", wives in order to marry women of foreign faiths. In the context of a fresh exegesis of the passage, a reinterpretation of the textually difficult verse 15a is offered. As it stands, the MT is most adequately rendered by: "And no one who has acted that way, has a remnant of spirit". With slight emendations, however, the text can be reconstructed as referring to God's creation of man and woman in Gen. i-ii. This reconstruction makes good sense in the context of the dispute in which Malachi is engaged, providing an additional argument against the dissolution of marriage. Though verse 16a does not contain a general prohibition of divorce, the reconstructed text of verse 15a should be understood as a general argument for the indissolubility of marriage.
Multiple roles foru-turn/ventral veinlessin the development ofDrosophilaPNS
Authors: Inbal Adi , Levanon Daniel , Salzberg Adi 
Published: April 2003

Most of the cells in the embryonic peripheral nervous system (PNS) of Drosophila are born in their final location. One known exception is the group of lateral chordotonal organs (lch5) whose precursors form in a dorsal position, yet the mature organs are located in the lateral PNS cluster. Mutations in the u-turn (ut) locus perturb the localization of lch5 neurons and result in a `dorsal chordotonals' phenotype. We show that ut is allelic to ventral veinless (vvl), also known as drifter. VVL, a POU-domain transcription factor, has been shown to participate in the development of tracheae and CNS in the embryo, and in wing development in the adult; however, its role in PNS development has not been described. Characterization of the `dorsal chordotonals' phenotype of vvl mutant embryos revealed that in the absence of VVL, cell fates within the lch5 lineage are determined properly and the entire organ is misplaced. Based on the positions of lch5 cells relative to each other in mutant embryos, and in normal embryos at different developmental stages, we propose a two-step model for lch5 localization. lch5 organs must first rotate to assume a correct polarity and are then stretched ventrally to their final position. In this process, VVL function is required in the ectoderm and possibly in the lch5 organs too.VVL is also expressed in developing external sensory organs in the embryo and in the adult. In the embryo, loss of VVL function results in increased apoptosis in specific es organs. Analysis of vvl mutant clones in adults revealed a requirement for VVL in the control of cell number within the bristle lineage.
Methylenetetrahydrofolate reductase (MTHFR): incidence of mutations C677T and A1298C in Brazilian population and its correlation with plasma homocysteine levels in spina bifida
Authors: Perez Ana Beatriz Alvarez , D'Almeida Vânia , Vergani Naja , de Oliveira Allan C. , de Lima Fernanda Teresa , Brunoni Decio 
Published: April 2003

AbstractHomocysteine (Hcy) is converted to cysteine or is remethylated to methionine by methylenetetrahydrofolate reductase (MTHFR). MTHFR plays a central role in the metabolism of folate. Two common polymorphisms in the MTHFR gene (C677T and A1298C) have been described and studies suggest that these polymorphisms are positively associated with the occurrence of spina bifida (SB). Among Brazilians, the incidence of 677T allele homozygosity is 4%. We compared Hcy levels with the genotypes obtained for the mutations C677T and A1298C in the gene MTHFR. Levels of plasma Hcy were higher in children with SB than in controls (average 7.95 vs. 5.55 (μmol/L); P < 0.001). There was no significant difference in the levels of Hcy for these childrens's mothers and controls (average 7.76 vs. 8.36 (μmol/L); P = 0.27). Eighty one (61.8%) of the affected children were white and 50 (38.2%) were non‐white. A similar ratio was observed in the mothers. In the control group, 51 children (40.5%) were white and 75 (59.5%) were non‐white, and 52 mothers (41.3%) were white and 74 (58.7%) were non‐white. There was no significant difference in the homozygous frequency for the mutated allele 677T among different racial groups. We obtained a prevalence of TT homozygosity of 10/131 (7.64%) in affected children and 13/126 (10.32%) in controls. With respect to the mutation A1298C, the homozygous prevalence for the wild allele was greater among non‐white individuals than in white individuals both in case and control groups. Hyperhomocysteinemia is a risk factor for SB. However, in our population, the increase in plasma levels of Hcy is not explained by the presence of the homozygous TT. It is possible that low folic acid intake combined with other genetic factors plays a more important role in the cause of this disease. © 2003 Wiley‐Liss, Inc.
Twin brothers with MIDAS syndrome and XX karyotype
Authors: Anguiano A. , Yang X. , Felix J.K. , Hoo J.J. 
Published: April 2003

AbstractTwin brothers with microphthalmia, facial dermal hypoplasia, sclerocornea, and supraventricular tachycardia, are reported. Their clinical features are compatible with MIDAS syndrome, a known X‐linked and hemizygous male lethal condition. Their karyotypes showed an XX sex chromosome modality with a subtle Xp/Yp translocation proven by the presence of SRY gene. The pregnancy was complicated with fetal supraventricular tachycardia, which was treated with digoxin prenatally. Postnatally, both twins required treatment with adenosine, digoxin, and propanolol to remain in normal sinus rhythm. The possible involvement of the heart, only in the form of cardiomyopathy with arrhythmia is emphasized. Both twins had a selective X‐inactivation of the derivative chromosome X with Xp/Yp translocation. © 2003 Wiley‐Liss, Inc.
Macrodystrophia lipomatosa of the feet and subcutaneous lipomas
Authors: Aydos S.E. , Fitoz S. , Bökesoy I. 
Published: April 2003

AbstractWe report on a girl aged 16 months with localized gigantism of the lower limb and widespread subcutaneous lipomas. This is the first case of macrodystrophia lipomatosa with lipomatous involvement in areas other than the involved limb. © 2003 Wiley‐Liss, Inc.