bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differences in Cell Activation byChlamydophila pneumoniaeandChlamydia trachomatisInfection in Human Endothelial Cells
Authors: Krüll M. , Kramp J. , Petrov T. , Klucken A. C. , Hocke A. C. , Walter C. , Schmeck B. , Seybold J. , Maass M. , Ludwig S. , Kuipers Jens G. , Suttorp N. , Hippenstiel S. 
Published: October 2004

ABSTRACTSeroepidemiological studies and demonstration of viable bacteria in atherosclerotic plaques have linkedChlamydophila pneumoniaeinfection to the development of chronic vascular lesions and coronary heart disease. In this study, we characterizedC. pneumoniae-mediated effects on human endothelial cells and demonstrated enhanced phosphorylation and activation of the endothelial mitogen-activated protein kinase (MAPK) family members extracellular receptor kinase (ERK1/2), p38-MAPK, and c-Jun-NH2kinase (JNK). Subsequent interleukin-8 (IL-8) expression was dependent on p38-MAPK and ERK1/2 activation as demonstrated by preincubation of endothelial cells with specific inhibitors for the p38-MAPK (SB202190) or ERK (U0126) pathway. Inhibition of either MAPK had almost no effect on intercellular cell adhesion molecule 1 (ICAM-1) expression. WhileChlamydia trachomatiswas also able to infect endothelial cells, it did not induce the expression of endothelial IL-8 or ICAM-1. These effects were specific for a direct stimulation with viableC. pneumoniaeand independent of paracrine release of endothelial cell-derived mediators like platelet-activating factor, NO, prostaglandins, or leukotrienes. Thus,C. pneumoniaetriggers an early signal transduction cascade in target cells that could lead to endothelial cell activation, inflammation, and thrombosis, which in turn may result in or promote atherosclerosis.
The Protective Effect of the
Mycobacterium bovis
BCG Vaccine Is Increased by Coadministration with the
Mycobacterium tuberculosis
72-Kilodalton Fusion Polyprotein Mtb72F in
M. tuberculosis
-Infected Guinea Pigs
Authors: Brandt Lise , Skeiky Yasir A. W. , Alderson Mark R. , Lobet Yves , Dalemans Wilfried , Turner Oliver C. , Basaraba Randall J. , Izzo Angelo A. , Lasco Todd M. , Chapman Philip L. , Reed Steven G. , Orme Ian M. 
Published: October 2004

ABSTRACT

A tuberculosis vaccine candidate consisting of a 72-kDa polyprotein or fusion protein based upon the Mtb32 and Mtb39 antigens of
Mycobacterium tuberculosis
and designated Mtb72F was tested for its protective capacity as a potential adjunct to the
Mycobacterium bovis
BCG vaccine in the mouse and guinea pig models of this disease. Formulation of recombinant Mtb72F (rMtb72F) in an AS02A adjuvant enhanced the Th1 response to BCG in mice but did not further reduce the bacterial load in the lungs after aerosol challenge infection. In the more stringent guinea pig disease model, rMtb72F delivered by coadministration with BCG vaccination significantly improved the survival of these animals compared to BCG alone, with some animals still alive and healthy in their appearance at >100 weeks post-aerosol challenge. A similar trend was observed with guinea pigs in which BCG vaccination was boosted by DNA vaccination, although this increase was not statistically significant due to excellent protection conferred by BCG alone. Histological examination of the lungs of test animals indicated that while BCG controls eventually died from overwhelming lung consolidation, the majority of guinea pigs receiving BCG mixed with rMtb72F or boosted twice with Mtb72F DNA had mostly clear lungs with minimal granulomatous lesions. Lesions were still prominent in guinea pigs receiving BCG and the Mtb72F DNA boost, but there was considerable evidence of lesion healing and airway remodeling and reestablishment. These data support the hypothesis that the coadministration or boosting of BCG vaccination with Mtb72F may limit the lung consolidation seen with BCG alone and may promote lesion resolution and healing. Collectively, these data suggest that enhancing BCG is a valid vaccination strategy for tuberculosis that is worthy of clinical evaluation.
The Hyphal and Yeast Forms ofCandida albicansBind the Complement Regulator C4b-Binding Protein
Authors: Meri T. , Blom A. M. , Hartmann A. , Lenk D. , Meri S. , Zipfel P. F. 
Published: October 2004

ABSTRACTCandida albicans, an important pathogenic yeast, activates all three pathways of the complement system. To understand how this yeast evades the effects of the activated system, we have analyzed the binding of the classical pathway inhibitor C4b-binding protein (C4BP) byC. albicans. Purified native as well as recombinant C4BP bound dose dependently to the yeast and hyphal forms, as shown by multiple methods, such as confocal microscopy, flow cytometry, a novel enzyme-linked immunosorbent assay, absorption from human serum, and direct binding assays with purified proteins. A prominent binding site was identified at the tip of the germ tube, a structure that is considered important for tissue penetration and pathogenesis. The binding site in C4BP was localized to the two N-terminal complement control protein domains by using recombinant deletion constructs and site-specific monoclonal antibodies. As the alternative pathway inhibitors factor H and FHL-1 also bind toC. albicans, the binding of all three plasma proteins was compared. Simultaneous binding of the classical regulator C4BP and the alternative pathway regulator factor H was demonstrated by confocal microscopy. In addition, FHL-1 competed for binding with C4BP, suggesting that these two related complement regulators bind to the same structures on the yeast surface. The surface-attached C4BP maintains its complement regulatory activities and inactivates C4b. The surface-attached human C4BP serves multiple functions relevant for immune evasion and likely pathogenicity. It inhibits complement activation at the yeast surface and, in addition, mediates adhesion ofC. albicansto host endothelial cells.
Mast Cell-Dependent Control ofGiardia lambliaInfections in Mice
Authors: Li Erqiu , Zhou Ping , Petrin Ziva , Singer Steven M. 
Published: October 2004

ABSTRACTMast cells are important for protective immunity to intestinal helminth infections and as mediators of allergic disease. Their role in protozoan infections is less well described. We have therefore analyzed mast cell responses and parasite control in mice infected with the protozoanGiardia lamblia. We also measured immunoglobulin A (IgA) responses to the parasite, as IgA can have a protective role in this model. c-kitw/wvmice failed to make parasite-specific IgA, mount a mast cell response, or eliminate the infection. Anti-c-kit-treated C57BL/6 mice had normal IgA responses, lacked mast cell responses, had reduced interleukin-6 (IL-6) mRNA in the small intestine, and failed to control the infection within 10 days. IL-9-deficient mice had a significant but reduced mast cell response and still controlled the infection within 2 weeks. Interestingly, IL-6-deficient mice had enhanced mast cell responses yet failed to rapidly control the infection. However, prevention of mast cell responses in IL-6-deficient mice by anti-c-kit treatment did not lead to parasite elimination. Both IL-6- and IL-9-deficient mice had normal IgA production. IL-6-deficient mice had significant serum levels of mast cell mediators, histamine and mast cell protease 1, following infection. Together, these results show that mast cells are important for the rapid control ofGiardiainfections in mice. Furthermore, they show that IL-6 is not necessary for these mast cell responses. Instead, they suggest that mast cell production of IL-6 appears to be important for control of this infection.
Functional Characterization of Two Type III Secretion Systems of
Vibrio parahaemolyticus
Authors: Park Kwon-Sam , Ono Takahiro , Rokuda Mitsuhiro , Jang Myoung-Ho , Okada Kazuhisa , Iida Tetsuya , Honda Takeshi 
Published: October 2004

ABSTRACT

Vibrio parahaemolyticus
, a gram-negative marine bacterium, is a worldwide cause of food-borne gastroenteritis. Recent genome sequencing of the clinical
V. parahaemolyticus
strain RIMD2210633 identified two sets of genes for the type III secretion system (TTSS), TTSS1 and TTSS2. Here, we constructed a series of mutant strains from RIMD2210633 to determine whether the two putative TTSS apparatus are functional. The cytotoxic activity of mutant strains having a deletion in one of the TTSS1 genes was significantly decreased compared with that of the parent and TTSS2-related mutant strains. In an enterotoxicity assay with the rabbit ileal loop test, intestinal fluid accumulation was diminished by deletion of the TTSS2-related genes while TTSS1-related mutants caused a level of fluid accumulation similar to that of the parent. VopD, a protein encoded in the proximity of the TTSS1 region and a homologue of the
Yersinia
YopD, was secreted in a TTSS1-dependent manner. In contrast, VopP, which is encoded by a pathogenicity island on chromosome 2 and is homologous to the
Yersinia
YopP, was secreted via the TTSS2 pathway. These results provide evidence that
V. parahaemolyticus
TTSSs function as secretion systems and may have a role in the pathogenicity of the organism. This is the first report of functional TTSSs in
Vibrio
species. The presence of TTSS apparatus gene homologues was demonstrated in other vibrios, such as
Vibrio alginolyticus
,
Vibrio harveyi
, and
Vibrio tubiashii
, suggesting that some other vibrios also contain TTSS and that the TTSS has a role in protein secretion in those organisms during interaction with eukaryotic cells.
Both Inducible Nitric Oxide Synthase and NADPH Oxidase Contribute to the Control of Virulent Phase ICoxiella burnetiiInfections
Authors: Brennan Robert E. , Russell Kasi , Zhang Guoquan , Samuel James E. 
Published: October 2004

ABSTRACTHost control ofCoxiella burnetiiinfections is believed to be mediated primarily by activated monocytes/macrophages. The activation of macrophages by cytokines leads to the production of reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI) that have potent antimicrobial activities. The contributions of ROI and RNI to the inhibition ofC. burnetiireplication were examined in vitro by the use of murine macrophage-like cell lines and primary mouse macrophages. A gamma interferon (IFN-γ) treatment of infected cell lines and primary macrophages resulted in an increased production of nitric oxide (NO) and hydrogen peroxide (H2O2) and a significant inhibition ofC. burnetiireplication. The inhibition of replication was reversed in the murine cell line J774.16 upon the addition of either the inducible nitric oxide synthase (iNOS) inhibitor NG-monomethyl-l-arginine (NGMMLA) or the H2O2scavenger catalase. IFN-γ-treated primary macrophages from iNOS−/−and p47phox−/−mice significantly inhibited replication but were less efficient at controlling infection than IFN-γ-treated wild-type macrophages. To investigate the contributions of ROI and RNI to resistance to infection, we performed in vivo studies, using C57BL/6 wild-type mice and knockout mice lacking iNOS or p47phox. Both iNOS−/−and p47phox−/−mice were attenuated in the ability to controlC. burnetiiinfection compared to wild-type mice. Together, these results strongly support a role for both RNI and ROI in the host control ofC. burnetiiinfection.
Shiga Toxin Binding to Isolated Porcine Tissues and Peripheral Blood Leukocytes
Authors: Winter Kellie R. K. , Stoffregen William C. , Dean-Nystrom Evelyn A. 
Published: October 2004

ABSTRACTShiga toxin (Stx) binding sites in porcine tissues and leukocytes were identified by the use of Stx overlay and anti-CD77/Gb3 immunoassays. Stx1 and Stx2 bound to similar tissue locations and leukocytes, although some differences were noted. Previously unreported Stx binding sites were identified in kidney tubules, intestinal lymphoid aggregates, sinusoidal liver cells, alveolar macrophages, and peripheral blood leukocytes.
Human Factor inStaphylococcus aureusNasal Carriage
Authors: Nouwen Jan , Boelens Hélène , van Belkum Alex , Verbrugh Henri 
Published: October 2004

ABSTRACTPersistent nasal carriers and noncarriers ofStaphylococcus aureuswere inoculated with a mixture of differentS. aureusstrains. The majority of noncarriers and nearly all persistent carriers returned to their original carrier state after artificial inoculation. Furthermore, the majority of persistent carriers tested positive again for their original resident strain. Using a human nasal inoculation model, we here demonstrate that the human factor is an important determinant ofS. aureusnasal carriage.
Moraxella catarrhalis
Coaggregates with
Streptococcus pyogenes
and Modulates Interactions of
S. pyogenes
with Human Epithelial Cells
Authors: Lafontaine Eric R. , Wall David , Vanlerberg Serena L. , Donabedian Haig , Sledjeski Darren D. 
Published: October 2004

ABSTRACT

The pathogens
Streptococcus pyogenes
and
Moraxella catarrhalis
colonize overlapping regions of the human nasopharynx. We have found that
M. catarrhalis
can dramatically increase
S. pyogenes
adherence to human epithelial cells and that species-specific coaggregation of these bacteria correlates with this enhanced adherence.
Streptococcus pneumoniae
-Induced Inhibition of Rat Ependymal Cilia Is Attenuated by Antipneumolysin Antibody
Authors: Hirst Robert A. , Mohammed Bashir J. , Mitchell Timothy J. , Andrew Peter W. , O'Callaghan Christopher 
Published: October 2004

ABSTRACT

Ciliated ependymal cells line the ventricular surfaces and aqueducts of the brain. In ex vivo experiments, pneumolysin caused rapid inhibition of the ependymal ciliary beat frequency and caused ependymal cell disruption. Wild-type pneumococci and pneumococci deficient in pneumolysin caused ciliary slowing, but penicillin lysis of wild-type, not pneumolysin-deficient, pneumococci increased the extent of ciliary inhibition. This effect was abolished by antipneumolysin antibody. Ependymal ciliary stasis by purified pneumolysin was also blocked by the addition of antipneumolysin monoclonal antibodies. These data show that antibiotic lysis of
Streptococcus pneumoniae
can be detrimental to the ciliated ependyma and that antipneumolysin antibody may have a therapeutic potential.
Cleavage of the N-Linked Oligosaccharide from the Surfaces of
Chlamydia
Species Affects Attachment and Infectivity of the Organisms in Human Epithelial and Endothelial Cells
Authors: Kuo Cho-chou , Lee Amy , Campbell Lee Ann 
Published: October 2004

ABSTRACT

Previous studies demonstrated that the high-mannose oligosaccharide N linked to the
Chlamydia
major outer membrane protein inhibited the attachment and infectivity of the organism. The present study showed that cleavage of the glycan with N-glycanase decreased the attachment and infectivity of chlamydial organisms in human epithelial and endothelial cells.
Variations in Barbour-Stoenner-Kelly Culture Medium Modulate Infectivity and Pathogenicity of
Borrelia burgdorferi
Clinical Isolates
Authors: Wang Guiqing , Iyer Radha , Bittker Susan , Cooper Denise , Small Jennifer , Wormser Gary P. , Schwartz Ira 
Published: October 2004

ABSTRACT

The effects of variations in Barbour-Stoenner-Kelly (BSK) medium on the infectivity and pathogenicity of
Borrelia burgdorferi
clinical isolates were assessed by retrospective and prospective studies using a murine model of Lyme borreliosis. Thirty of 35 (86%) mice infected with any of six virulent
B. burgdorferi
clinical isolates grown in a BSK-H medium developed clinically apparent arthritis. By contrast, arthritis was observed in only 25 of 60 (42%) mice inoculated with two of these
B. burgdorferi
strains grown in a different lot of BSK-H medium (
P
< 0.001). In a prospective study, mice inoculated with a
B. burgdorferi
clinical isolate grown in a BSK medium prepared in-house produced significantly greater disease than those injected with the same isolate cultured in BSK-H medium (
P
< 0.05). The attenuated pathogenicity is not due to the loss of plasmids during in vitro cultivation. The data suggest that variations in BSK medium have a significant impact on the infectivity and pathogenicity of
B. burgdorferi
clinical isolates.
Identification of Genes Transcribed byActinobacillus pleuropneumoniaein Necrotic Porcine Lung Tissue by Using Selective Capture of Transcribed Sequences
Authors: Baltes Nina , Gerlach Gerald F. 
Published: October 2004

ABSTRACTGenes expressed byActinobacillus pleuropneumoniaein necrotic porcine lung tissue were identified by selective capture of transcribed sequences analysis. In total, 46 genes were identified, 20 of which have been previously reported to be associated with in vivo expression or virulence inA. pleuropneumoniaeor in other organisms.
Human Galectin-3 PromotesTrypanosoma cruziAdhesion to Human Coronary Artery Smooth Muscle Cells
Authors: Kleshchenko Yuliya Y. , Moody Tapria N. , Furtak Vyacheslav A. , Ochieng Josiah , Lima Maria F. , Villalta Fernando 
Published: October 2004

ABSTRACTHuman galectin-3 binds to the surface ofTrypanosoma cruzitrypomastigotes and human coronary artery smooth muscle (CASM) cells. CASM cells express galectin-3 on their surface and secrete it. Exogenous galectin-3 increased the binding ofT. cruzito CASM cells. Trypanosome binding to CASM cells was enhanced when eitherT. cruzior CASM cells were preincubated with galectin-3. Cells stably transfected with galectin-3 antisense show a dramatic decrease in galectin-3 expression and very littleT. cruziadhesion to cells. The addition of galectin-3 to these cells restores their initial capacity to bind to trypanosomes. Thus, host galectin-3 expression is required forT. cruziadhesion to human cells and exogenous galectin-3 enhances this process, leading to parasite entry.
Interleukin-15-Deficient Mice Develop Protective Immunity toToxoplasma gondii
Authors: Lieberman Linda A. , Villegas Eric N. , Hunter Christopher A. 
Published: October 2004

ABSTRACTPrevious studies have suggested an important role for interleukin-15 (IL-15) in resistance to and memory forToxoplasma gondiiinfection. The studies presented here reveal that IL-15 is not required for infection-induced expansion of NK or CD8+T cells. Furthermore, IL-15−/−mice develop long-term protective immunity to this pathogen.
In Vitro and In Vivo Evaluation of Staphylococcal Superantigen Peptide Antagonists
Authors: Rajagopalan Govindarajan , Sen Moon M. , David Chella S. 
Published: October 2004

ABSTRACTSuperantigen peptide antagonists failed to block T-cell activation and cytokine production as well as toxic shock induced by staphylococcal enterotoxin B (SEB) in HLA class II transgenic mice. They also failed to inhibit the binding of SEB to HLA class II molecules as well as activation of human T lymphocytes in vitro.
Identification of
Neisseria meningitidis
Genetic Loci Involved in the Modulation of Phase Variation Frequencies
Authors: Alexander Heather L. , Rasmussen Andrew W. , Stojiljkovic Igor 
Published: October 2004

ABSTRACT

It has been proposed that increased phase variation frequencies in
Neisseria meningitidis
augment transmissibility and invasiveness. A
Himar1 mariner
transposon mutant library was constructed in serogroup A
N. meningitidis
and screened for clones with increased phase variation frequencies. Insertions increasing the frequency of slippage events within mononucleotide repeat tracts were identified in three known phase variation-modulating genes (
mutS
,
mutL
, and
uvrD
), as well as six additional loci (
pilP
,
fbpA
,
fbpB
, NMA1233, and two intergenic regions). The implications of these insertion mutations are discussed.
Streptococcus mutans
Surface α-Enolase Binds Salivary Mucin MG2 and Human Plasminogen
Authors: Ge Jingping , Catt Diana M. , Gregory Richard L. 
Published: October 2004

ABSTRACT

Matrix-assisted laser desorption ionization-time of flight mass spectrometry analysis identified enolase as a cell surface component of
Streptococcus mutans
, which was confirmed by enzyme-linked immunosorbent assay, Western blotting, and transmission electron microscopy. Surface enolase was demonstrated to bind to human plasminogen and salivary mucin MG2. The results suggested a role for enolase in
S. mutans
attachment, clearance, or breach of the bloodstream barrier.
HARDWARE PROTOTYPES OF A BOOLEAN NEURAL NETWORK AND THE SIMULATED ANNEALING OPTIMIZATION METHOD
Authors: NIITTYLAHTI JARKKO 
Published: October 2004

Boolean Neural Network is a neural network that operates with binary weight values of “1” and “0”. Otherwise it is formally analogous to the Multilayer Perceptron (MLP).1 Simulated Annealing is a stochastic optimization method that is suitable for performing nonlinear multivariable optimization tasks. Training a Boolean Neural Network is a well-suited problem to this algorithm. However, the Simulated Annealing method is computationally heavy, which makes the training procedure slow. The training speed can be improved by using custom designed hardware for the whole system including the optimization method and the neural network. Hardware prototypes of a Boolean Neural Network and the Simulated Annealing optimization method have been designed using discrete components. The Boolean Neural Network implementation is basically a dynamically configurable feedforward network of Boolean logic gates of two inputs. The Simulated Annealing implementation is a general purpose hardware tool for multivariable optimization tasks. Here it is applied to do supervised training of the Boolean Neural Network hardware.
WHAT CAUSES ION CHANNEL PROTEINS TO FLUCTUATE OPEN AND CLOSED?
Authors: LIEBOVITCH LARRY S. , TODOROV ANGELO T. 
Published: October 2004

Ion channels in the cell membrane spontaneously switch from states that are closed to the flow of ions such as sodium, potassium, and chloride to states that are open to the flow of these ions. The durations of times that an individual ion channel protein spends in the closed and open states can be measured by the patch clamp technique. We explore two basic issues about the molecular properties of ion channels: 1) If the switching between the closed and open state is an inherently random event, what does the patch clamp data tell us about the structure or motions in the ion channel protein? 2) Is this switching random?
NOISE IN MODELS OF NEUROLOGICAL AND PSYCHIATRIC DISORDERS
Authors: SPITZER MANFRED , NEUMANN MANFRED 
Published: October 2004

The concept of noise has only recently been applied to modelling neuropsychiatric disorders. Two examples of such models are presented. 1. A phantom limb is a neurological condition after the amputation of an extremity. It consists of sensations of the presence of the lost limb and has been attributed to cortical as well as non-cortical mechanisms. A neural network model of phantom limbs is proposed which can parsimoniously account for a large number of clinical features and recent findings of cortical map plasticity after deafferentation. In trained self-organizing feature maps, deafferentation was simulated. Reorganization is shown to be driven by input noise. According to the model, the production of input noise by the deafferented primary sensory neuron drives cortical reorganization in amputees. No such noise is generated and/or conducted to the cortex in paraplegics. 2. Several clinical features of schizophrenia have been related to the ratio of signal to noise in neuronal information processing. In particular, dopamine — which has been implicated in the causation of schizophrenia for decades — has been proposed to modulate signal-to-noise ratio. Data are presented which suggest that schizophrenic thought disorder is the result of a hypodopaminergic state and concomitant increased effects of noise in semantic information processing. Possible functions of noise in the nervous systems are discussed.