bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hepatitis E Virus Immunoglobulin G Antibodies in Different Populations in Campinas, Brazil
Authors: Gonçales Neiva S. L. , Pinho João Renato R. , Moreira Regina C. , Saraceni Cláudia P. , Spina Ângela M. M. , Stucchi Raquel B. , Filho Aírton D. Ribeiro , Magna Luís A. , Gonçales Júnior Fernando L. 
Published: July 2002

ABSTRACT
The seroprevalence of anti-hepatitis E virus (HEV) antibodies was investigated by enzyme immunoassay in 205 volunteer blood donors, 214 women who attended a center for anonymous testing for human immunodeficiency virus (HIV) infection, and 170 hospital employees in Campinas, a city in southeastern Brazil. The prevalence of anti-HEV antibodies ranged from 2.6% (3 of 117) in health care professionals to 17.7% (38 of 214) in women who considered themselves at risk for HIV. The prevalence of anti-HEV antibodies in health care professionals was not significantly different from that in healthy blood donors (3.0%, 5 of 165) and blood donors with raised alanine aminotransferase levels (7.5%, 3 of 40). The prevalence of anti-HEV antibodies (13.2%, 7 of 53) in cleaning service workers at a University hospital was similar to that among women at risk for HIV infection. These results suggest that HEV is circulating in southeastern Brazil and that low socioeconomic status is an important risk factor for HEV infection in this region.
Feed a Cold, Starve a Fever?
Authors: van den Brink Gijs R. , van den Boogaardt Daniëlle E. M. , van Deventer Sander J. H. , Peppelenbosch Maikel P. 
Published: July 2002

ABSTRACTAn English old wives’ tale advises us to “feed a cold and starve a fever.” Here we report that the nutritional status modulates the T helper 1 (Th1)-Th2 balance of activated T cells in human volunteers. Food intake resulted in increased levels of gamma interferon production, whereas food deprivation stimulated interleukin-4 release.
Comparison of Murex Single-Use Diagnostic System with Traditional Enzyme Immunoassay for Detection of Exposure to Human Immunodeficiency Virus
Authors: Martin Christin A. , Keren David F. 
Published: July 2002

ABSTRACT
Because a retrospective study detected 13 negative Western blots out of 38 single-use diagnostic system (SUDS)-positive cases over a 1-year period, we performed a prospective study to compare the performance of the SUDS test with that of enzyme immunoassay (EIA). Of 888 SUDS-tested sera, 875 (98.4%) were both SUDS and EIA negative and 5 (0.6%) were SUDS, EIA, and Western blot positive. The rate of SUDS-positive samples decreased from 3.16/month in the retrospective study to 1.33/month in the prospective study. The immunoassays had sensitivities and specificities of 100 and 99.7 (SUDS) and 100 and 99.4% (traditional EIA), respectively. In laboratories with experienced personnel, the SUDS test performs as well as the EIA as a screen for infection with the human immunodeficiency virus.
CD4+T-Cell Subsets That Mediate Immunological Memory toMycobacterium tuberculosisInfection in Mice
Authors: Andersen Peter , Smedegaard Birgitte 
Published: July 2002

ABSTRACTWe have studied CD4+T cells that mediate immunological memory to an intravenous infection withMycobacterium tuberculosis. The studies were conducted with a mouse model of memory immunity in which mice are rendered immune by a primary infection followed by antibiotic treatment and rest. Shortly after reinfection, tuberculosis-specific memory cells were recruited from the recirculating pool, leading to rapidly increasing precursor frequencies in the liver and a simultaneous decrease in the blood. A small subset of the infiltrating T cells was rapidly activated (<20 h) and expressed high levels of intracellular gamma interferon and the T-cell activation markers CD69 and CD25. These memory effector T cells expressed intermediate levels of CD45RB and were heterogeneous with regard to the L-selectin and CD44 markers. By adoptive transfer into nude mice, the highest level of resistance to a challenge withM. tuberculosiswas mediated by CD45RBhigh,l-selectinhigh, CD44lowcells. Taken together, these two lines of evidence support an important role for memory cells which have reverted to a naive phenotype in the long-term protection againstM. tuberculosis.
Two Allelic Forms of the Aureolysin Gene (
aur
) within
Staphylococcus aureus
Authors: Sabat Artur , Kosowska Klaudia , Poulsen Knud , Kasprowicz Andrzej , Sekowska Agnieszka , van den Burg Bertus , Travis James , Potempa Jan 
Published: July 2002

ABSTRACT

Proteinases of
Staphylococcus aureus
are emerging as potential virulence factors which may be involved in the pathogenecity of staphylococcal diseases. We describe here the structure of the gene encoding the metalloproteinase referred to as aureolysin. This gene occurs in two allelic forms and is strongly conserved among
S. aureus
strains, implying the possibility that the proteinase may have important housekeeping functions.
Immunization with Recombinant
Helicobacter pylori
Urease in Specific-Pathogen-Free Rhesus Monkeys (
Macaca mulatta
)
Authors: Solnick Jay V. , Canfield Don R. , Hansen Lori M. , Torabian Sima Z. 
Published: July 2002

ABSTRACT

Immunization with urease can protect mice from challenge with
Helicobacter pylori
, though results vary depending on the particular vaccine, challenge strain, and method of evaluation. Unlike mice, rhesus monkeys are naturally colonized with
H. pylori
and so may provide a better estimate of vaccine efficacy in humans. The purpose of this study was to examine the effectiveness of
H. pylori
urease as a vaccine in specific-pathogen (
H. pylori
)-free rhesus monkeys. Monkeys raised from birth and documented to be free of
H. pylori
were vaccinated with orogastric (
n
= 4) or intramuscular (
n
= 5) urease. Two control monkeys were sham vaccinated. All monkeys were challenged with a rhesus monkey-derived strain of
H. pylori
, and the effects of vaccination were evaluated by use of quantitative cultures of gastric tissue, histology, and measurement of serum immunoglobulin G (IgG) and salivary IgA. Despite a humoral immune response, all monkeys were infected after
H. pylori
challenge, and there were no differences in the density of colonization. Immunization with urease therefore does not fully protect against challenge with
H. pylori
. An effective vaccine to prevent
H. pylori
infection will require different or more likely additional antigens, as well as improvements in the stimulation of the host immune response.
Major Carbohydrate Antigen ofEchinococcus multilocularisInduces an Immunoglobulin G Response Independent of αβ+CD4+T Cells
Authors: Dai Wen Juan , Hemphill Andrew , Waldvogel Andreas , Ingold Katrin , Deplazes Peter , Mossmann Horst , Gottstein Bruno 
Published: July 2002

ABSTRACTEchinococcus multiloculariscauses alveolar echinococcosis, one of the most lethal helminthic (accidental) infections in humans, as the life cycle predominantly includes wildlife rodents as intermediate hosts. The physical barrier between the proliferating parasitic metacestode and the host tissue is the acellular laminated layer (LL), which is characterized by its rich high-molecular-weight polysaccharide composition. Conversely to a crude protein-rich vesicular fluid antigen, a major carbohydrate antigen of the LL—the Em2(G11) antigen—did not stimulate murine T-cell proliferation in vitro. In fact, the persistent metacestode growth and antigenic stimulation induced a Th2 shift in vivo following conventional infection by intraperitoneal inoculation of 100 metacestode vesicles into C57/BL6 mice. Concurrently, the expression of Th1 cytokines (interleukin-2 and gamma interferon) remained persistently low until the late stage of chronic infection. In comparison to a recombinant proteinic II/3 antigen, the specific immunoglobulin G (IgG) response against the Em2(G11) antigen (including all IgG isotypes) maintained persistently low avidity. Furthermore, the Em2(G11) antigen induced a specific IgM and IgG response in T-cell-deficient athymic nude, TCRβ−/−, major histocompatibility complex class II (MHCII)−/−(CD4-deficient), and CD40−/−mice. The Em2(G11)-specific IgG synthesized in nude TCRβ−/−and MHCII−/−mice was predominantly of the IgG3 and IgG2a isotypes and of the IgG3 and IgG2b isotypes in CD40−/−mice. This finding suggested that in vivo, the IgG response to major carbohydrate antigen Em2(G11) ofE. multiloculariscould take place independently of αβ+CD4+T cells and in the absence of CD40-CD40 ligand interactions; thus, the Em2(G11) antigen of the acellular LL represents a T-cell-independent antigen. Functionally, the encapsulating LL, and especially its major carbohydrate antigen, Em2(G11), seems to be one of the key factors in the parasite's survival strategy and acts by modulating the host immune response by virtue of its T-cell-independent nature.
Identification of a Locus Involved in Systemic Dissemination of
Yersinia enterocolitica
Authors: Nelson Kristin M. , Young Glenn M. , Miller Virginia L. 
Published: July 2002

ABSTRACT

A putative LysR-type transcriptional activator, Hre20, was identified previously in an in vivo expression technology screen designed to identify factors which are expressed early during infection by
Yersinia enterocolitica
(G. M. Young and V. L. Miller, Mol. Microbiol. 25:319–328, 1997). An insertion in
hre20
, now designated
rscR
, resulted in increased splenic dissemination of bacteria during infection in a BALB/c mouse model. A nonpolar mutation was generated in
rscR
, and examination of this strain in the BALB/c mouse model demonstrated that the mutation in
rscR
was responsible for the increased dissemination to the spleen that was seen in the original experiments. RscR is homologous to the LysR family of transcriptional regulators; thus, a screen was undertaken to identify genes regulated by RscR. A strain containing an insertion in the chromosomal
rscR
gene and carrying
rscR
on a plasmid under the control of the inducible
araBAD
promoter was mutagenized with an mTn
5
Km-2 transposon containing a promoterless
lacZY
. Eighteen insertions were identified which appeared to respond to levels of RscR, and these were classified into four allelic groups based on Southern blot hybridization analysis. Representative members were sequenced from three allelic groups. Sequencing revealed insertions in an ORF with no known homologues, a homologue of OmpF of
Serratia marcescens
, and a locus (designated
rscBAC
) with similarity to the
hmwABC
locus of
Haemophilus influenzae
. The
hmwABC
locus promotes adherence of
H. influenzae
to host cells (S. J. Barenkamp and J. W. St. Geme III, Infect. Immun. 62:3320–3328, 1994; J. W. St. Geme III, S. Falkow, and S. J. Barenkamp, Proc. Natl. Acad. Sci. USA 90:2875–2879, 1993). A strain containing a deletion mutant of
rscA
, the
hmwA
homologue, exhibits increased splenic dissemination of bacteria during infection in a BALB/c mouse model, similar to the
rscR
mutant. This suggests that the phenotype of an
rscR
mutant is due to the loss of RscA.
CD8+-T-Cell Depletion Ameliorates Circulatory Shock inPlasmodium berghei-Infected Mice
Authors: Chang Wun-Ling , Jones Steven P. , Lefer David J. , Welbourne Tomas , Sun Guang , Yin Lijia , Suzuki Hodaka , Huang Jian , Granger D. Neil , van der Heyde Henri C. 
Published: July 2002

ABSTRACTThePlasmodium berghei-infected mouse model is a well-recognized model for human cerebral malaria. Mice infected withP. bergheiexhibit (i) metabolic acidosis (pH < 7.3) associated with elevated plasma lactate concentrations, (ii) significant (P< 0.05) vascular leakage in their lungs, hearts, kidneys, and brains, (ii) significantly (P< 0.05) higher cell and serum glutamate concentrations, and (iv) significantly (P< 0.05) lower mean arterial blood pressures. Because these complications are similar to those of septic shock, the simplest interpretation of these findings is that the mice develop shock brought on by theP. bergheiinfection. To determine whether the immune system and specifically CD8+T cells mediate the key features of shock duringP. bergheimalaria, we depleted CD8+T cells by monoclonal antibody (mAb) treatment and assessed the complications of malarial shock.P. berghei-infected mice depleted of CD8+T cells by mAb treatment had significantly reduced vascular leakage in their hearts, brains, lungs, and kidneys compared with infected controls treated with rat immunoglobulin G. CD8-depleted mice were significantly (P< 0.05) protected from lactic acidosis, glutamate buildup, and diminished HCO3−levels. Although the blood pressure decreased in anti-CD8 mAb-treated mice infected withP. berghei, the cardiac output, as assessed by echocardiography, was similar to that of uninfected control mice. Collectively, our results indicate that (i) pathogenesis similar to septic shock occurs during experimentalP. bergheimalaria, (ii) respiratory distress with lactic acidosis occurs duringP. bergheimalaria, and (iii) most components of circulatory shock are ameliorated by depletion of CD8+T cells.
Inflammation and Clearance ofChlamydia trachomatisin Enteric and Nonenteric Mucosae
Authors: Igietseme Joseph U. , Portis John L. , Perry Linda L. 
Published: July 2002

ABSTRACTImmunization(s) fostering the induction of genital mucosa-targeted immune effectors is the goal of vaccines against sexually transmitted diseases. However, it is uncertain whether vaccine administration should be based on the current assumptions about the common mucosal immune system. We investigated the relationship between mucosal sites of infection, infection-induced inflammation, and immune-mediated bacterial clearance in mice using the epitheliotropic pathogenChlamydia trachomatis. Chlamydial infection of the conjunctival, pulmonary, or genital mucosae stimulated significant changes in tissue architecture with dramatic up-regulation of the vascular addressin, VCAM, a vigorous mixed-cell inflammatory response with an influx of α4β1+T cells, and clearance of bacteria within 30 days. Conversely, intestinal mucosa infection was physiologically inapparent, with no change in expression of the local MAdCAM addressin, no VCAM induction, no histologically detectable inflammation, and no tissue pathology. Microbial clearance was complete within 60 days in the small intestine but bacterial titers remained at high levels for at least 8 months in the large intestine. These findings are compatible with the notion that VCAM plays a functional role in recruiting cells to inflammatory foci, and its absence from the intestinal mucosa contributes to immunologic homeostasis at that site. Also, expression of type 1 T cell-mediated immunity to intracellularChlamydiamay exhibit tissue-specific variation, with the rate and possibly the mechanism(s) of clearance differing between enteric and nonenteric mucosae. The implications of these data for the common mucosal immune system and the delivery of vaccines against mucosal pathogens are discussed.
Gender Is a Major Factor in Determining the Severity of Mycoplasma Respiratory Disease in Mice
Authors: Yancey Anthony L. , Watson Harold L. , Cartner Sam C. , Simecka Jerry W. 
Published: July 2002

ABSTRACT

Gender is a significant factor in determining the susceptibility to and severity of pulmonary diseases in both humans and animals. Murine respiratory mycoplasmosis (MRM), due to
Mycoplasma pulmonis
infection, is an excellent animal model for evaluation of the role of various host factors on the development of acute or chronic inflammatory lung diseases. MRM has many similarities to mycoplasma respiratory disease in humans. The purpose of the present study was to determine whether gender has a significant impact on lung disease due to
M. pulmonis
infection in mice. It was demonstrated that male mice consistently developed more severe disease in the lung parenchyma than did female mice. There was no gender difference in disease severity along the airways or any difference in mycoplasma numbers in lungs of male and female mice. Furthermore, surgical removal of reproductive organs reduced the severity of mycoplasma disease and the numbers of mycoplasma organisms recovered from lungs. Thus, gender plays a significant role in determining the severity of
M. pulmonis
disease. In fact, the gender of the host was a major factor in determining whether an acute or chronic inflammatory lung disease developed after infection with
M. pulmonis
.
Secreted Variant of Nucleoside Diphosphate Kinase from the Intracellular Parasitic Nematode
Trichinella spiralis
Authors: Gounaris Kleoniki , Thomas Simon , Najarro Pilar , Selkirk Murray E. 
Published: July 2002

ABSTRACT

The molecular components involved in the survival of the parasitic nematode
Trichinella spiralis
in an intracellular environment are poorly characterized. Here we demonstrate that infective larvae secrete a nucleoside diphosphate kinase when maintained in vitro. The secreted enzyme forms a phosphohistidine intermediate and shows broad specificity in that it readily accepts γ-phosphate from both ATP and GTP and donates it to all nucleoside and deoxynucleoside diphosphate acceptors tested. The enzyme was partially purified from culture medium by ATP affinity chromatography and identified as a 17-kDa protein by autophosphorylation and reactivity with an antibody to a plant-derived homologue. Secreted nucleoside diphosphate kinases have previously been identified only in prokaryotic organisms, all of them bacterial pathogens. The identification of a secreted variant of this enzyme from a multicellular eukaryote is very unusual and is suggestive of a role in modulating host cell function.
Analysis of Mechanisms Associated with Loss of Infectivity of Clonal Populations of
Borrelia burgdorferi
B31MI
Authors: McDowell John V. , Sung Shian Ying , Labandeira-Rey Maria , Skare Jon T. , Marconi Richard T. 
Published: July 2002

ABSTRACT

Numerous studies have provided suggestive evidence that the loss of plasmids correlates with the loss of infectivity of the Lyme disease spirochetes. In this study we have further investigated this correlation. Clonal populations were obtained from the skin of a mouse infected for 3 months with a clonal population of
Borrelia burgdorferi
B31MI. The complete plasmid compositions of these populations were determined using a combination of PCR and Southern hybridization. The infectivities of clones differing in plasmid composition were tested using the C3H-HeJ murine model for Lyme disease. While several clones were found to be noninfectious, a correlation between the loss of a specific plasmid and loss of infectivity in the clones analyzed in this report was not observed. While it is clear from recent studies that the loss of some specific plasmids results in attenuated virulence, this study demonstrates that additional mechanisms also contribute to the loss of infectivity.
Improved Pattern for Genome-Based Screening Identifies Novel Cell Wall-Attached Proteins in Gram-Positive Bacteria
Authors: Janulczyk Robert , Rasmussen Magnus 
Published: July 2002

ABSTRACTWith a large number of sequenced microbial genomes available, tools for identifying groups or classes of proteins have become increasingly important. Here we present an improved pattern for the identification of cell wall-attached proteins (CWPs), a group of proteins with diverse and important functions in gram-positive bacteria. This tripartite pattern is based on analysis of 65 previously described cell wall-attached proteins and takes into account the three principal requirements for cell wall sorting; a sortase target region (LPXTGX), a membrane-spanning region, and a charged stop-transfer tail. In five different genomes of gram-positive bacteria, the tripartite pattern identified a total of 35 putative CWPs, 19 of which were novel. The specificity and sensitivity of the tripartite pattern are higher than those of the classical pattern, which is based solely on the sortase target region. Several putative CWPs with atypical sortase target regions were identified. In the complete genome of the important human pathogenStreptococcus pyogenes, the tripartite pattern identified 14 putative CWPs. Seven of the putativeS. pyogenesproteins were novel, and two of these were a 5′ nucleotidase and a pullulanase. This study represents the first whole-genome screening for CWPs, and we conclude that the tripartite pattern is highly suitable for this purpose. Identification of CWPs using this pattern offers important possibilities in the study of the pathogenesis and physiology of gram-positive bacteria.
Concurrent Upregulation of Urokinase Plasminogen Activator Receptor and CD11b during Tuberculosis and Experimental Endotoxemia
Authors: Juffermans Nicole P. , Dekkers Pascale E. P. , Verbon Annelies , Speelman Peter , van Deventer Sander J. H. , van der Poll Tom 
Published: July 2002

ABSTRACTPatients with tuberculosis had higher expression of monocyte urokinase receptor (uPAR) and CD11b than controls. In vitro, lipoarabinomannan and lipopolysaccharide (LPS) fromEscherichia colishared the ability to enhance uPAR and CD11b expression on monocytes and granulocytes. In healthy volunteers, LPS induced increases in monocyte and granulocyte uPAR and CD11b.
Intracellular Survival of
Neisseria gonorrhoeae
in Male Urethral Epithelial Cells: Importance of a Hexaacyl Lipid A
Authors: Post Deborah M. B. , Phillips Nancy J. , Shao Jian Q. , Entz David D. , Gibson Bradford W. , Apicella Michael A. 
Published: July 2002

ABSTRACT

Neisseria gonorrhoeae
is a strict human pathogen that invades and colonizes the urogenital tracts of males and females. Lipooligosaccharide (LOS) has been shown to play a role in gonococcal pathogenesis. The acyl transferase MsbB is involved in the biosynthesis of the lipid A portion of the LOS. In order to determine the role of an intact lipid A structure on the pathogenesis of
N. gonorrhoeae
, the
msbB
gene was cloned and sequenced, a deletion and insertion mutation was introduced into
N. gonorrhoeae
, and the mutant strain was designated 1291A11K3. Mass spectrometric analyses of 1291A11K3 LOS determined that this mutation resulted in a pentaacyl rather than a hexaacyl lipid A structure. These analyses also demonstrated an increase in the phosphorylation of lipid A and an increase in length of the oligosaccharide of a minor species of the
msbB
LOS. The interactions of this mutant with male urethral epithelial cells (uec) were examined. Transmission and scanning electron microscopy studies indicated that the
msbB
mutants formed close associations with and were internalized by the uec at levels similar to those of the parent strain. Gentamicin survival assays performed with 1291A11K3 and 1291 bacteria demonstrated that there was no difference in the abilities of the two strains to adhere to uec; however, significantly fewer 1291A11K3 bacteria than parent strain bacteria were recovered from gentamicin-treated uec. These studies suggest that the lipid A modification in the
N. gonorrhoeae msbB
mutant may render it more susceptible to innate intracellular killing mechanisms when internalized by uec.