bluuebunny/crossref_metadata_2025_split huggingface dataset:
Molecular Aspects of Biogenesis of
Escherichia coli
Dr Fimbriae: Characterization of DraB-DraE Complexes
Authors: Piątek Rafał , Zalewska Beata , Kolaj Olga , Ferens Michał , Nowicki Bogdan , Kur Józef 
Published: December 2004

ABSTRACT

The Dr hemagglutinin of uropathogenic
Escherichia coli
is a fimbrial homopolymer of DraE subunits encoded by the
dra
operon. The
dra
operon includes the
draB
and
draC
genes, whose products exhibit homology to chaperone-usher proteins involved in the biogenesis of surface-located polymeric structures. DraB is one of the periplasmic proteins belonging to the superfamily of PapD-like chaperones. It possesses two conserved cysteine residues characteristic of the FGL subfamily of Caf1M-like chaperones. In this study we obtained evidence that DraB cysteines form a disulfide bond in a mature chaperone and have the crucial function of forming the DraB-DraE binary complex. Expression experiments showed that the DraB protein is indispensable in the folding of the DraE subunit to a form capable of polymerization. Accumulation of DraB-DraE
n
oligomers, composed of head-to-tail subunits and the chaperone DraB, was observed in the periplasm of a recombinant
E. coli
strain which expressed DraB and DraE (but not DraC). To investigate the donor strand exchange mechanism during the formation of DraE oligomers, we constructed a series of DraE N-terminal deletion mutants. Deletion of the first three N-terminal residues of a potential donor strand resulted in a DraE protein lacking an oligomerization function. In vitro data showed that the DraE disulfide bond was not needed to form a binary complex with the DraB chaperone but was essential in the polymerization process. Our data suggest that assembly of Dr fimbriae requires a chaperone-usher pathway and the donor strand exchange mechanism.
Kinetics and Avidity of Antibodies Evoked by Heptavalent Pneumococcal Conjugate Vaccines PncCRM and PncOMPC in the Finnish Otitis Media Vaccine Trial
Authors: Ekström Nina , Åhman Heidi , Verho Jouko , Jokinen Jukka , Väkeväinen Merja , Kilpi Terhi , Käyhty Helena 
Published: December 2004

ABSTRACT
The licensure of new pneumococcal conjugate vaccines (PCVs) relies on immunogenicity data. When defining correlates of protection, vaccine efficacy data must be included. In the FinOM Vaccine Efficacy Trial, the PncOMPC vaccine showed an efficacy profile similar to that of the licensed PncCRM vaccine despite different antibody responses after primary and booster vaccinations. We determined antibody kinetics and avidities in a subgroup of infants participating in the FinOM trial. A total of 166 infants in three vaccine groups were immunized at 2, 4, 6, and 12 months of age with 7-valent PCV, PncCRM or PncOMPC, or hepatitis B vaccine. Concentrations of serum immunoglobulin G (IgG) against pneumococcal capsular polysaccharides were determined at 2, 4, 6, 7, 12, 13, and 24 months of age, and the avidity index (AI) to serotypes 6B, 19F, and 23F were determined at 7, 12, 13, and 24 months of age by enzyme immunoassay. Both PCVs were highly immunogenic, but they demonstrated different kinetics of antibody response; the concentration of IgG against serotypes 6B, 19F, and 23F declined faster after the third and fourth doses of vaccine in the PncCRM group than in the PncOMPC group. For both PCVs, the mean AI of anti-6B and -23F, but not of anti-19F, increased during the follow-up, which is in line with serotype-specific protection in the FinOM trial. Our data suggest that the kinetics and avidities of antibodies should be considered, in addition to antibody responses, when defining correlates of protection.
Transient Neutralization of Tumor Necrosis Factor Alpha Can Produce a Chronic Fungal Infection in an Immunocompetent Host: Potential Role of Immature Dendritic Cells
Authors: Herring Amy C. , Falkowski Nicole R. , Chen Gwo-Hsiao , McDonald Rod A. , Toews Galen B. , Huffnagle Gary B. 
Published: December 2004

ABSTRACTThe mechanisms underlying induction of immune dysregulation and chronic fungal infection by a transient tumor necrosis factor alpha (TNF-α) deficiency remain to be defined. The objective of our studies was to determine the potential contribution of neutropenia and immature dendritic cells to the immune deviation. Administration of an anti-TNF-α monoclonal antibody at day 0 neutralized TNF-α only during the first week of a pulmonaryCryptococcus neoformansinfection. Transient neutralization of TNF-α resulted in transient depression of interleukin-12 (IL-12), monocyte chemotactic protein 1 (MCP-1), and gamma interferon (IFN-γ) production but permanently impaired long-term clearance of the infection from the lungs even after the levels of these cytokines increased and a vigorous inflammatory response developed. Early neutrophil recruitment was defective in the absence of TNF-α. However, as demonstrated by neutrophil depletion studies, this did not account for the decrease in IL-12 and IFN-γ levels and did not play a role in establishing chronic pulmonary cryptococcal infection. Transient TNF-α neutralization also produced a deficiency in CD11c+MHC II+cells and IL-12 in the lymph nodes, potentially implicating a defect in mature dendritic cell trafficking. Transfer of cryptococcal antigen-pulsed immature dendritic cells into naïve mice prior to intratracheal challenge resulted in the development of a nonprotective immune response toC. neoformansthat was similar to that observed in anti-TNF-α-treated mice (increased IL-4, IL-5, and IL-10 levels, pulmonary eosinophilia, and decreased clearance). Thus, stimulation of an antifungal response by immature dendritic cells can result in an immune deviation similar to that produced by transient TNF-α deficiency, identifying a new mechanism by which a chronic fungal infection can occur in an immunocompetent host.
Enterococcus faecalis
Mammalian Virulence-Related Factors Exhibit Potent Pathogenicity in the
Arabidopsis thaliana
Plant Model
Authors: Jha Ajay K. , Bais Harsh P. , Vivanco Jorge M. 
Published: December 2004

ABSTRACT

Some pathogenic bacteria belong to a large, diverse group of species capable of infecting plants, animals, and humans.
Enterococcus faecalis
is an opportunistic human pathogen capable of infecting patients with a deficient immune system. Here we report that three
E. faecalis
strains (FA-2-2, V583, and OG1RF) are capable of infecting the leaves and roots of the model plant species
Arabidopsis thaliana
, causing plant mortality 7 days postinoculation. We found that
E. faecalis
pathogenesis in
A. thaliana
leaves is determined by the following series of events: attachment to leaf surface, entry through stomata or wounds, and colonization in intercellular spaces, leading to rotting and to the disruption of plant cell wall and membrane structures. The three
E. faecalis
strains colonize the roots of
A. thaliana
by forming a mosaic of large clusters of live bacteria on the root surface, as observed by scanning electron microscopy, phase-contrast microscopy, and fluorescence microscopy. To dissect the involvement of mammalian virulence-related factors in plant pathogenicity, we tested
E. faecalis
mutant strains Δ
fsrA
(TX5240), Δ
fsrB
(TX5266), Δ
fsrC
(TX5242), Δ
gelE
(TX5264), and Δ
sprE
(TX5243), which correspond to virulence factors involved in pathogenesis in different animal models. Two
E. faecalis
virulence-related factors that play an important role in mammalian and nematode models of infection, a putative quorum-sensing system (Δ
fsrB
) and serine protease (Δ
sprE
), were also found to be important for plant pathogenesis. The development of an
E. faecalis
-
A. thaliana
model system could potentially be used to circumvent certain inherent limitations that an animal model imposes on the identification and study of virulence factors. Furthermore, our study suggests an evolutionary crossover of virulence factors in plant, animal, and nematode pathogenesis.
CXCR3 and Its Ligands Participate in the Host Response toBordetella bronchisepticaInfection of the Mouse Respiratory Tract but Are Not Required for Clearance of Bacteria from the Lung
Authors: Widney Daniel P. , Hu Yan , Foreman-Wykert Amy K. , Bui Kim C. , Nguyen Tam T. , Lu Bao , Gerard Craig , Miller Jeff F. , Smith Jeffrey B. 
Published: December 2004

ABSTRACTIntranasal inoculation of mice withBordetella bronchisepticaproduces a transient pneumonia that is cleared over several weeks in a process known to require both neutrophils and lymphocytes. In this study, we evaluated the roles of the chemokines MIG (CXCL9), IP-10 (CXCL10), and I-TAC (CXCL11) and their common receptor, CXCR3. Following bacterial inoculation, message expression of interleukin-1 (IL-1), IL-6, and the neutrophil-attracting chemokines KC, LIX, and MIP-2 was rapidly induced, with maximal expression found at 6 h. In contrast, message expression of gamma interferon, MIG, IP-10, and I-TAC peaked at 2 days. Expression of all of these chemokines and cytokines returned to near baseline by 5 days, despite the persistence of high levels of live bacteria at this time. Induced MIG, IP-10, and I-TAC protein expression was localized in areas of inflammation at 2 to 3 days and was temporally associated with increased levels of CXCR3+lymphocytes in bronchoalveolar lavage fluid. There was no increase in mortality in mice lacking CXCR3. However, the clearance of bacteria from the lung and trachea was delayed, and the recruitment of lymphocytes and NK cells was slightly decreased, for CXCR3−/−mice relative to CXCR3+/+mice. We conclude that the CXCR3 receptor-ligand system contributes to pulmonary host defense inB. bronchisepticainfection by recruiting lymphocytes and NK cells into the lung.
Mucosal
FOXP3
-Expressing CD4
+
CD25
high
Regulatory T Cells in
Helicobacter pylori
-Infected Patients
Authors: Lundgren Anna , Strömberg Erika , Sjöling Åsa , Lindholm Catharina , Enarsson Karin , Edebo Anders , Johnsson Erik , Suri-Payer Elisabeth , Larsson Pia , Rudin Anna , Svennerholm Ann-Mari , Lundin B. Samuel 
Published: December 2004

ABSTRACT

Helicobacter pylori
chronically colonizes the stomach and duodenum and causes peptic ulcers or gastric adenocarcinoma in 10 to 20% of infected individuals. We hypothesize that the inability of patients to clear
H. pylori
infections is a consequence of active suppression of the immune response. Here we show that
H. pylori
-infected individuals have increased frequencies of CD4
+
CD25
high
T cells in both the stomach and duodenal mucosa compared to uninfected controls. These cells have the phenotype of regulatory T cells, as they express
FOXP3
, a key gene for the development and function of regulatory T cells, as well as high levels of the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) protein. In contrast, mucosal CD4
+
CD25
low
and CD4
+
CD25
−
cells express little
FOXP3
mRNA and low levels of the CTLA-4 protein. Mucosal CD4
+
CD25
high
T cells are present in individuals with asymptomatic
H. pylori
infections as well as in duodenal ulcer patients. The frequencies of CD4
+
CD25
high
cells are also increased in the stomachs of
H. pylori
-infected patients with gastric adenocarcinoma, particularly in cancer-affected tissues. These findings suggest that regulatory T cells may suppress mucosal immune responses and thereby contribute to the persistence of
H. pylori
infections.
Endurance training and testing with the ball in young elite soccer players
Authors: Chamari K , Hachana Y , Kaouech F , Jeddi R , Moussa-Chamari I , Wisløff U 
Published: December 2004

Background:The aerobic capacity of soccer players substantially influences their technical performance and tactical choices. Thus, the assessment of soccer players’ aerobic performance should be of interest for soccer coaches in order to evaluate and improve their endurance training sessions. In this study, we present a new test to assess aerobic performance in soccer by means of a specific dribbling track: the Hoff test. We further determined whether improvement in maximal oxygen uptake was reflected in increased distance covered in the Hoff test.Methods:We tested 18 male soccer players (14 years old) both in the laboratory and using the Hoff test before and after 8 weeks of soccer training.Results:The distance covered in the Hoff test correlated significantly with maximum oxygen uptake, and improved by 9.6% during the 8 week training period, while maximum oxygen uptake and running economy improved by 12 and 10%, respectively. Backward multiple regression showed maximum oxygen uptake to be the main explanatory variable for the distance covered in the Hoff test.Conclusion:The present study demonstrated a significant correlation between laboratory testing of VO2maxand performance in the Hoff test. Furthermore, training induced improvements in VO2maxwere reflected in improved performance in the Hoff test. We suggest that it should be a goal for active U-15 soccer players to cover more than 2100 metres in the Hoff test, as this requires a VO2maxof above 200 ml/kg0.75/min, which should serve as a minimum in modern soccer.
Riverine spawning and reproductive segregation in a lacustrine cyprinid species flock, facilitated by homing?
Authors: Palstra Arjan , de Graaf Martin , Sibbing Ferdinand 
Published: December 2004

Abstract
This paper aims at assessing the reproductive segregation within the endemic Barbus (renamed Labeobarbus) species flock of Lake Tana (Ethiopia). Migration, followed by temporal and spatial reproductive segregation in the upstream tributaries of two inflowing rivers was studied systematically over the 1999 and 2000 spawning seasons. Physical events that may trigger lacustrine migration and characterise suitability of spawning grounds were analysed. Six species migrate 30-40 km upstream Gumara River during declining flow, just after the rainy season. Spawning occurs in the well-oxygenated gravel beds of four Gumara tributaries. Eight 'large barb' species were absent from the rivers, or found only incidentally, thus segregating them at a macro-spatial scale from the six river-spawners. The missing species spawn either in the lake or in other rivers not sampled. Long distance migration and species-specific spawning sites suggest that homing may have facilitated reproductive isolation and speciation. A fine-tuning between homing and gonad development is suggested since females reach spawning maturity only as they arrive at the spawning grounds. This study provides convincing evidence for reproductive segregation, and contributes in unravelling the evolution of this unique Labeobarbus species flock. Collective migration and riverine spawning of six Labeobarbus species makes them very vulnerable for overfishing at the spawning areas.
Phylogeny, origin and biogeography of catfishes: support for a Pangean origin of 'modern teleosts' and reexamination of some Mesozoic Pangean connections between the Gondwanan and Laurasian supercontinents
Authors: Diogo Rui 
Published: December 2004

AbstractThe wide geographical distribution of the mainly freshwater catfishes has long intrigued the scientific community. This work provides a new insight into the phylogeny and the puzzling biogeographical distribution of catfishes. The important implications for teleost biogeography and plate tectonics are discussed. The results of the author's cladistic study on catfish higher level phylogeny, together with a revision of the data available concerning different fields such as palaeobiogeography, phylogeny, ecology and molecular biology, as well as the growing evidence supporting the existence of some remaining Pangean connections between Gondwana and Laurasia extending into the Early Cretaceous, strongly support a rather complex biogeographic scenario with multiple pre-drift and post-drift continental dispersions, vicariances, and, possibly, some marine migrations. According to this scenario: 1) catfishes originated in the South American region at a moment when there were still some remaining Pangean connections between Gondwana and Laurasia; 2) after this, there was a relatively rapid pre-drift continental dispersion of several, but not all, main groups of Siluriformes from the South-American region to Africa and other Gondwanan areas, with some of those groups succeeding in radiating ulteriorly via the remaining continental Pangean connections between Gondwana and Laurasia to this latter super-continent; 3) the final separation between Laurasia and Gondwana, and posteriorly between the regions constituting each of these super-continents, contributed to important vicariant events; 4) this scenario was still further complicated by numerous events such as the collision of India with Asia, the re-establishment of certain land connections between previously separated continents (e.g., between the Americas), and eventually also by some marine migrations, thus explaining the highly complex biogeographical distribution of the Siluriformes. In sustaining such a scenario, this work thus supports that, contrary to what is often accepted, some groups of 'modern teleosts' did have a Pangean origin.
Role of Rap1 in promoting sickle red blood cell adhesion to laminin via BCAM/LU
Authors: Murphy Meghan M. , Zayed Mohamed A. , Evans Allyson , Parker Carol E. , Ataga Kenneth I. , Telen Marilyn J. , Parise Leslie V. 
Published: December 2004

AbstractVaso-occlusion is a hallmark of sickle cell disease. Agonist-induced activation of sickle red blood cells (SS RBCs) promotes their adhesion to vascular proteins, potentially contributing to vasoocclusion. Previously, we described a cyclic adenosine monophosphate (cAMP)-dependent increase in SS RBC adhesion to laminin. Here, we investigated whether Rap1, a small guanosine triphosphatase (GTPase) known to promote integrin-mediated adhesion in other cells, was involved in this signaling pathway. We found that agonists known to induce cAMP signaling promoted the GTP-bound, active state of Rap1 in SS RBCs. The cAMP-dependent exchange factor Epac (exchange protein directly activated by cAMP) is a likely upstream activator of Rap1, since Epac is present in these cells and the Epac-specific cAMP analog 8CPT-2-Me (8-(4-cholorophenylthio)-2′-O-methyl-cAMP) activated Rap1 and promoted SS RBC adhesion to laminin. This 8CPT-2-Me-stimulated adhesion was integrin independent, since it was insensitive to RGD peptide or antibodies against the only known integrin on SS RBCs, α4β1. However, this adhesion was completely inhibited by either a soluble version of basal cell adhesion molecule/Lutheran (BCAM/LU) or a BCAM/LU adhesion-blocking anti-body. Surprisingly, 8CPT-2-Me-activated Rap1 did not promote SS RBC adhesion to a known α4β1 ligand, vascular cell adhesion molecule 1 (VCAM-1). These results demonstrate that Epac-induced Rap1 activation in SS RBCs promotes BCAM/LU-mediated adhesion to laminin. Thus, Epac-mediated Rap1 activation may represent an important signaling pathway for promoting SS RBC adhesion. (Blood. 2005;105:3322-3329)
Determinants of ABH expression on human blood platelets
Authors: Cooling Laura L. W. , Kelly Kathleen , Barton James , Hwang Debbie , Koerner Theodore A. W. , Olson John D. 
Published: December 2004

AbstractPlatelets express ABH antigens, which can adversely effect platelet transfusion recovery and survival in ABH-incompatible recipients. To date, there has been no large, comprehensive study comparing specific donor factors with ABH expression on platelet membranes and glycoconjugates. We studied ABH expression in 166 group A apheresis platelet donors by flow cytometry, Western blotting, and thin layer chromatography relative to donor age, sex, A1/A2 subgroup, and Lewis phenotype. Overall, A antigen on platelet membranes, glycoproteins, and glycosphingolipids was linked to an A1 red blood cell (RBC) phenotype. Among A1 donors, platelet ABH varied significantly between donors (0%-87%). Intradonor variability, however, was minimal, suggesting that platelet ABH expression is a stable, donor-specific characteristic, with 5% of A1 donors typing as either ABH high- or low-expressers. Group A2 donors, in contrast, possessed a Bombay-like phenotype, lacking both A and H antigens. Unlike RBCs, ABH expression on platelets may be determined primarily by H-glycosyltransferase (FUT1) activity. Identification of A2 and A1 low expressers may increase the availability and selection of crossmatched and HLA-matched platelets. Platelets from group A2 may also be a superior product for patients undergoing A/O major mismatch allogeneic progenitor cell transplantation. (Blood. 2005;105:3356-3364)
Antibody responses to H-Y minor histocompatibility antigens correlate with chronic graft-versus-host disease and disease remission
Authors: Miklos David B. , Kim Haesook T. , Miller Katherine H. , Guo Luxuan , Zorn Emmanuel , Lee Stephanie J. , Hochberg Ephraim P. , Wu Catherine J. , Alyea Edwin P. , Cutler Corey , Ho Vincent , Soiffer Robert J. , Antin Joseph H. , Ritz Jerome 
Published: December 2004

AbstractMinor histocompatibility antigens (mHAs) are known targets of donor T cells after allogeneic hematopoietic stem cell transplantation (HSCT). In contrast, B-cell responses to mHAs have not been extensively characterized and the clinical significance of antibodies to mHAs is unknown. We tested 121 patients who underwent HSCT and 134 healthy donors for immunoglobulin G (IgG) antibodies against 5 mHAs encoded by genes on the Y chromosome (DBY, UTY, ZFY, RPS4Y, and EIF1AY). Antibodies to at least one H-Y protein developed in 52% of male patients with female donors compared with 8.7% of male patients with male donors (P &lt; .0001), and in 41.4% of healthy females compared with 7.8% of healthy males (P &lt; .0001). H-Y antibodies develop 4 to 12 months after transplantation and persist for long periods. The clinical significance of H-Y antibodies was characterized in 75 male patients with hematologic malignancies who received stem cells from female donors (F → M HSCT). The presence of H-Y antibodies correlated with chronic graft-versus-host disease (GVHD) by univariate (odds ratio [OR] = 15.5; P &lt; .0001) and multivariable logistic regression analysis (OR = 56.5; P &lt; .0001). Antibody response to Y-chromosome encoded histocompatibility antigens (H-Y antigens) was also associated with maintenance of disease remission (P &lt; .0001). B cells may provide a new target for immune intervention in chronic GVHD.
CD38 and CD100 lead a network of surface receptors relaying positive signals for B-CLL growth and survival
Authors: Deaglio Silvia , Vaisitti Tiziana , Bergui Luciana , Bonello Lisa , Horenstein Alberto L. , Tamagnone Luca , Boumsell Laurence , Malavasi Fabio 
Published: December 2004

AbstractThis work addresses the question whether CD38, a negative prognostic marker in B-cell chronic lymphocytic leukemia (B-CLL), plays a role in neoplastic B-cell growth and survival. We show that CD38+ B-CLL cells bind to murine fibroblasts transfected with the CD31 ligand. The interaction triggers an extensive remodeling of the B-CLL membrane, with relocalization of BCR/CD19 to the CD38/CD31 contact areas, and it also increases cell survival and proliferation. A second event is the up-modulation of the survival receptor CD100, restricted to proliferating cells, and a concomitant decrease of CD72 (low-affinity CD100 ligand and negative regulator of immune responses). The most efficient signals are delivered through sequential interactions between CD38/CD31 and CD100/plexin-B1 (high-affinity CD100 ligand), as inferred by coculture experiments using specific transfectants and blocking monoclonal antibodies (mAbs). The finding that nurselike cells from B-CLL patients express CD31 and plexin-B1, which deliver growth and survival signals to CD38+/CD100+ B-CLL cells, further confirms the model proposed. These findings show that a set of normal receptors and ligands ruling physiologic signaling pathways in B lymphocytes becomes detrimental when expressed in the context of B-CLL cells, ultimately leading to the generation of a tumor reservoir.