bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inflammatory Lipoproteins Purified from a Toxigenic and Arthritogenic Strain ofMycoplasma arthritidisAre Dependent on Toll-Like Receptor 2 and CD14
Authors: Hasebe Akira , Mu Hong-Hua , Washburn Leigh R. , Chan Fok V. , Pennock Nathan D. , Taylor Michael L. , Cole Barry C. 
Published: February 2007

ABSTRACTMycoplasma arthritidisis a naturally occurring murine pathogen, and the disease model has been used extensively to understand inflammatory mechanisms. Recently, Triton X-114 extracts of a virulent strain ofM. arthritidiswere found to be more potent in activating macrophages than were those from an avirulent strain, suggesting a role in disease. Here, octyl glucoside extraction of cells was used to identify four distinct bioactive moieties, with molecular masses of ∼41, 37, 34, and 17 kDa. Their bioactivities were resistant to proteinase K but were destroyed by alkaline hydrolysis and oxidation. As for MALP-2, all were dependent upon Toll-like receptor 2, but unlike MALP-2, they were also dependent upon CD14. TheM. arthritidislipoproteins exhibited infrared absorbances at 2,900 cm−1and 1,662 cm−1, similar to those seen in Pam3-Cys-Ser-(Lys)4. Edman degradation failed to reveal N-terminal sequences, suggesting that they were blocked and therefore might be triacylated. However, mass spectrometry of fragments revealed that the 41-kDa moiety, which binds to serum apolipoprotein A-1, had similarity with the recently described MlpD lipoprotein ofM. arthritidis.
Carboxypeptidases B of
Anopheles gambiae
as Targets for a
Plasmodium falciparum
Transmission-Blocking Vaccine
Authors: Lavazec C. , Boudin C. , Lacroix R. , Bonnet S. , Diop A. , Thiberge S. , Boisson B. , Tahar R. , Bourgouin C. 
Published: February 2007

ABSTRACT

Anopheles gambiae
is the major African vector of
Plasmodium falciparum
, the most deadly species of human malaria parasite and the most prevalent in Africa. Several strategies are being developed to limit the global impact of malaria via reducing transmission rates, among which are transmission-blocking vaccines (TBVs), which induce in the vertebrate host the production of antibodies that inhibit parasite development in the mosquito midgut. So far, the most promising components of a TBV are parasite-derived antigens, although targeting critical mosquito components might also successfully block development of the parasite in its vector. We previously identified
A. gambiae
genes whose expression was modified in
P. falciparum
-infected mosquitoes, including one midgut carboxypeptidase gene,
cpbAg1.
Here we show that
P. falciparum
up-regulates the expression of
cpbAg1
and of a second midgut carboxypeptidase gene,
cpbAg2
, and that this up-regulation correlates with an increased carboxypeptidase B (CPB) activity at a time when parasites establish infection in the mosquito midgut. The addition of antibodies directed against CPBAg1 to a
P. falciparum
-containing blood meal inhibited CPB activity and blocked parasite development in the mosquito midgut. Furthermore, the development of the rodent parasite
Plasmodium berghei
was significantly reduced in mosquitoes fed on infected mice that had been immunized with recombinant CPBAg1. Lastly, mosquitoes fed on anti-CPBAg1 antibodies exhibited reduced reproductive capacity, a secondary effect of a CPB-based TBV that could likely contribute to reducing
Plasmodium
transmission. These results indicate that
A. gambiae
CPBs could constitute targets for a TBV that is based upon mosquito molecules.
Immunoglobulin G Antibody Reactivity to a Group A
Plasmodium falciparum
Erythrocyte Membrane Protein 1 and Protection from
P. falciparum
Malaria
Authors: Magistrado Pamela A. , Lusingu John , Vestergaard Lasse S. , Lemnge Martha , Lavstsen Thomas , Turner Louise , Hviid Lars , Jensen Anja T. R. , Theander Thor G. 
Published: February 2007

ABSTRACT

Variant surface antigens (VSA) on the surface of
Plasmodium falciparum
-infected red blood cells play a major role in the pathogenesis of malaria and are key targets for acquired immunity. The best-characterized VSA belong to the
P. falciparum
erythrocyte membrane protein 1 (PfEMP1) family. In areas where
P. falciparum
is endemic, parasites causing severe malaria and malaria in young children with limited immunity tend to express semiconserved PfEMP1 molecules encoded by group A
var
genes. Here we investigated antibody responses of Tanzanians who were 0 to 19 years old to PF11_0008, a group A PfEMP1. PF11_0008 has previously been found to be highly transcribed in a nonimmune Dutch volunteer experimentally infected with NF54 parasites. A high proportion of the Tanzanian donors had antibodies against recombinant PF11_0008 domains, and in children who were 4 to 9 years old the presence of antibodies to the PF11_0008 CIDR2β domain was associated with reduced numbers of malaria episodes. These results indicate that homologues of PF11_0008 are present in
P. falciparum
field isolates and suggest that PF11_0008 CIDR2β-reactive antibodies might be involved in protection against malaria episodes.
Effect of Farnesol on a Mouse Model of Systemic Candidiasis, Determined by Use of a
DPP3
Knockout Mutant of
Candida albicans
Authors: Navarathna Dhammika H. M. L. P. , Hornby Jacob M. , Krishnan Navasona , Parkhurst Anne , Duhamel Gerald E. , Nickerson Kenneth W. 
Published: February 2007

ABSTRACT

This work extends our previous observation that the fungus
Candida albicans
secretes micromolar levels of farnesol and that accumulation of farnesol in vitro prevents the yeast-to-mycelium conversion in a quorum-sensing manner. What does farnesol do in vivo? The purpose of this study was to determine the role of farnesol during infection with a well-established mouse model of systemic candidiasis with
C. albicans
A72 administered by tail vein injection. This question was addressed by altering both endogenous and exogenous farnesol. For endogenous farnesol, we created a knockout mutation in
DPP3
, the gene encoding a phosphatase which converts farnesyl pyrophosphate to farnesol. This mutant (KWN2) produced six times less farnesol and was ca. 4.2 times less pathogenic than its SN152 parent. The strain with
DPP3
reconstituted (KWN4) regained both its farnesol production levels and pathogenicity. These mutants (KWN1 to KWN4) retained their full dimorphic capability. With regard to exogenous farnesol, farnesol was administered either intraperitoneally (i.p.) or orally in the drinking water. Mice receiving
C. albicans
intravenously and farnesol (20 mM) orally had enhanced mortality (
P
< 0.03). Similarly, mice (
n
= 40) injected with 1.0 ml of 20 mM farnesol i.p. had enhanced mortality (
P
< 0.03), and the onset of mortality was 30 h sooner than for mice which received a control injection without farnesol. The effect of i.p. farnesol was more pronounced (
P
< 0.04) when mice were inoculated with a sublethal dose of
C. albicans
. These mice started to die 4 days earlier, and the percent survival on day 6 postinoculation (p.i.) was five times lower than for mice receiving
C. albicans
with control i.p. injections. In all experiments, mice administered farnesol alone or Tween 80 alone remained normal throughout a 14-day observation period. Finally, beginning at 12 h p.i., higher numbers of
C. albicans
cells were detected in kidneys from mice receiving i.p. farnesol than in those from mice receiving control i.p. injections. Thus, reduced endogenous farnesol decreased virulence, while providing exogenous farnesol increased virulence. Taken together, these data suggest that farnesol may play a role in disease pathogenesis, either directly or indirectly, and thus may represent a newly identified virulence factor.
Cloning, Expression, and Characterization of the Superantigen Streptococcal Pyrogenic Exotoxin G from
Streptococcus dysgalactiae
Authors: Zhao Jizi , Hayashi Tomohito , Saarinen Susanna , Papageorgiou Anastassios C. , Kato Hidehito , Imanishi Ken'ichi , Kirikae Teruo , Abe Ryo , Uchiyama Takehiko , Miyoshi-Akiyama Tohru 
Published: February 2007

ABSTRACT

We identified seven novel variants of streptococcal pyrogenic exotoxin G (SPEGG), a superantigen, in
Streptococcus dysgalactiae
subsp.
dysgalactiae
or
equisimilis
isolates from clinical cases of infection in humans and animals. Phylogenetic analysis of the SPEGG variants indicated two clades in the dendrogram: one composed of variants derived from the bacteria isolated from the humans and the other composed of variants from the bacteria isolated from the animals. Bovine peripheral blood mononuclear cells (PBMCs) were stimulated effectively by recombinant SPEGGs (rSPEGGs) expressed in
Escherichia coli
, while human PBMCs were not stimulated well by any of the rSPEGGs tested. SPEGGs selectively stimulated bovine T cells bearing Vβ1,10 and Vβ4. Bovine serum showed reactivity to the rSPEGG proteins. These results indicated that SPEGGs have properties as superantigens, and it is likely that SPEGGs play a pathogenic role in animals.
Dependence of Macrophage Phagocytic Efficacy on Antibody Concentration
Authors: Macura Nataša , Zhang Tong , Casadevall Arturo 
Published: February 2007

ABSTRACT

Macrophages ingest the fungus
Cryptococcus neoformans
only in the presence of opsonins, and this provides a remarkably clean system for the detailed analysis of phagocytosis. This system is also unusual in that antibody-mediated phagocytosis involves ingestion through both Fc and complement receptors in the absence of complement. Mathematical modeling was used to analyze and explain the experimental data that the macrophage phagocytic index increased with increasing doses of antibody despite saturating concentrations and declined at high concentrations. A model was developed that explains the increase in phagocytic index with increasing antibody doses, differentiates among the contributions from Fc and complement receptors, and provides a tool for estimating antibody concentrations that optimize efficacy of phagocytosis. Experimental results and model calculations revealed that blocking of Fc receptors by excess antibody caused a reduction in phagocytic index but increased phagocytosis through complement receptors rapidly compensated for this effect. At high antibody concentrations, a further reduction in phagocytic index was caused by interference with complement receptor ingestion as a consequence of saturation of the fungal capsule. The ability of our model to predict the antibody dose dependence of the macrophage phagocytic efficacy for
C. neoformans
strongly suggest that the major variables that determine the efficacy of this process have been identified. The model predicts that the affinity constant of the opsonic antibody for the Fc receptor and the association-dissociation constant of antibody from the microbial antigen are critical parameters determining the efficacy of phagocytosis.
Solitary Intestinal Lymphoid Tissue Provides a Productive Port of Entry for
Salmonella enterica
Serovar Typhimurium
Authors: Halle Stephan , Bumann Dirk , Herbrand Heike , Willer Yvonne , Dähne Sabrina , Förster Reinhold , Pabst Oliver 
Published: February 2007

ABSTRACT

Oral infection of mice with
Salmonella enterica
serovar Typhimurium results in the colonization of Peyer's patches, triggering a vigorous inflammatory response and immunopathology at these sites. Here we demonstrate that in parallel to Peyer's patches a strong inflammatory response occurs in the intestine, resulting in the appearance of numerous inflammatory foci in the intestinal mucosa. These foci surround small lymphoid cell clusters termed solitary intestinal lymphoid tissue (SILT).
Salmonella
can be observed inside SILT at early stages of infection, and the number of infected structures matches the number of inflammatory foci arising at later time points. Infection leads to enlargement and morphological destruction of SILT but does not trigger de novo formation of lymphoid tissue. In conclusion, SILT, a lymphoid compartment mostly neglected in earlier studies, represents a major site for
Salmonella
invasion and ensuing mucosal pathology.
Evidence for Widespread Epithelial Damage and Coincident Production of Monocyte Chemotactic Protein 1 in a Murine Model of Intestinal Ricin Intoxication
Authors: Yoder J. Marina , Aslam Rabia U. , Mantis Nicholas J. 
Published: February 2007

ABSTRACTThe development of small-animal models is necessary to understand host responses and immunity to emerging infectious diseases and potential bioterrorism agents. In this report we have characterized a murine model of intestinal ricin intoxication. Ricin administered intragastrically (i.g.) to BALB/c mice at doses ranging from 1 to 10 mg/kg of body weight induced dose-dependent morphological changes in the proximal small intestine (i.e., duodenum), including widespread villus atrophy and epithelial damage. Coincident with epithelial damage was a localized increase in monocyte chemotactic protein 1, a chemokine known to be associated with inflammation of the intestinal mucosa. Immunity to intestinal ricin intoxication was achieved by immunizing mice i.g. with ricin toxoid and correlated with elevated levels of antitoxin mucosal immunoglobulin A (IgA) and serum IgG antibodies. We expect that this model will serve as a valuable tool in identifying the inflammatory pathways and protective immune responses that are elicited in the intestinal mucosa following ricin exposure and will prove useful in the evaluation of antitoxin vaccines and therapeutics.
Regulation of Exoprotein Gene Expression by the
Staphylococcus aureus cvfB
Gene
Authors: Matsumoto Yasuhiko , Kaito Chikara , Morishita Daisuke , Kurokawa Kenji , Sekimizu Kazuhisa 
Published: February 2007

ABSTRACT

We previously reported that the
cvfB
gene (SA1223) of
Staphylococcus aureus
is responsible for the virulence of this pathogenic bacterium. We show here that the
cvfB
gene regulates exoprotein gene expression. In a
cvfB
gene deletion mutant, hemolysin, DNase, and protease production were decreased, whereas protein A expression was increased. The amount of RNAIII, the transcript from the P3 promoter in the
agr
locus that regulates the expression of various virulence factors, was also reduced in the
cvfB
mutant. In addition, P2 and P3 promoter activity in the
agr
locus was decreased in the mutant. Under the genetic background of the
agr
-null mutation,
cvfB
gene disruption decreased the production levels of DNase and protease. Moreover, the
cvfB
and
agr
double mutant was less virulent than the
agr
mutant in silkworms. These results suggest that the
cvfB
gene product contributes to the expression of virulence factors and to pathogenicity
via
both
agr
-dependent and
agr
-independent pathways.
Induction of Human β-Defensin 2 by the ProbioticEscherichia coliNissle 1917 Is Mediated through Flagellin
Authors: Schlee Miriam , Wehkamp Jan , Altenhoefer Artur , Oelschlaeger Tobias A. , Stange Eduard F. , Fellermann Klaus 
Published: February 2007

ABSTRACTHuman β-defensin 2 (hBD-2) is an inducible antimicrobial peptide synthesized by the epithelium to counteract bacterial adherence and invasion. Proinflammatory cytokines, as well as certain bacterial strains, have been identified as potent endogenous inducers. Recently, we have found that hBD-2 induction by probioticEscherichia coliNissle 1917 was mediated through NF-κB- and AP-1-dependent pathways. The aim of the present study was to identify the responsible bacterial factor.E. coliNissle 1917 culture supernatant was found to be more potent than the pellet, indicating a soluble or shed factor. Chemical analysis demonstrated the factor to be heat resistant and proteinase digestible. SeveralE. coliNissle 1917 deletion mutants were constructed and tested for their ability to induce hBD-2 expression in Caco-2 cells. Deletion mutants for flagellin specifically exhibited an impaired immunostimulatory capacity. Reinsertion of the flagellin gene restored the induction capacity to normal levels. Isolated flagellin fromE. coliNissle 1917 and fromSalmonella entericaserovar Enteritidis induced hBD-2 mRNA significantly in contrast to the flagellin of the apathogenicE. colistrain ATCC 25922. H1 flagellin antiserum abrogated hBD-2 expression induced by flagellin as well asE. coliNissle 1917 supernatant, confirming that flagellin is the major stimulatory factor ofE. coliNissle 1917.
The SAG1Toxoplasma gondiiSurface Protein Is Not Required for Acute Ocular Toxoplasmosis in Mice
Authors: Charles Elizabeth , Callegan Michelle C. , Blader Ira J. 
Published: February 2007

ABSTRACTThe SAG1Toxoplasma gondiisurface protein stimulates acute ileitis. To determine whether SAG1 is also important in the eye, wild-type or SAG1 knockout parasites were injected intravitreally into mice. No differences in retinal damage or parasite growth were observed, indicating that unlike the case for the intestine, factors besides SAG1 are important for retinal damage.
Mice Lacking CD21 and CD35 Proteins Mount Effective Immune Responses againstBorrelia burgdorferiInfection
Authors: Jacobson Amanda C. , Ma Ying , Zachary James F. , Weis Janis J. , Weis John H. 
Published: February 2007

ABSTRACTCD21/35−/−mice, deficient in CD21 and CD35 (complement receptors 2 and 1, respectively), were infected withBorrelia burgdorferito assess the role of these receptors in a chronic bacterial infection. Although CD21/35−/−mice on both C57BL/6 and BALB/c backgrounds produced lessB. burgdorferi-specific antibodies than did wild-type mice, spirochete levels and arthritis severity were similar.
Resistance toPseudomonas aeruginosaChronic Lung Infection Requires Cystic Fibrosis Transmembrane Conductance Regulator-Modulated Interleukin-1 (IL-1) Release and Signaling through the IL-1 Receptor
Authors: Reiniger Nina , Lee Martin M. , Coleman Fadie T. , Ray Christopher , Golan David E. , Pier Gerald B. 
Published: February 2007

ABSTRACTInnate immunity is critical for clearingPseudomonas aeruginosafrom the lungs. In response toP. aeruginosainfection, a central transcriptional regulator of innate immunity—NF-κB—is translocated within 15 min to the nuclei of respiratory epithelial cells expressing wild-type (WT) cystic fibrosis (CF) transmembrane conductance regulator (CFTR).P. aeruginosaclearance from lungs is impaired in CF, and rapid NF-κB nuclear translocation is defective in cells with mutant or missing CFTR. We used WT and mutantP. aeruginosaand strains of transgenic mice lacking molecules involved in innate immunity to identify additional mediators required forP. aeruginosa-induced rapid NF-κB nuclear translocation in lung epithelia. We found neither Toll-like receptor 2 (TLR2) nor TLR4 nor TLR5 were required for this response. However, both MyD88-deficient mice and interleukin-1 receptor (IL-1R)-deficient mice failed to rapidly translocate NF-κB to the nuclei of respiratory epithelial cells in response toP. aeruginosa. Cultured human bronchial epithelial cells rapidly released IL-1β in response toP. aeruginosa; this process was maximized by expression of WT-CFTR and dramatically muted in cells with ΔF508-CFTR. The IL-1R antagonist blockedP. aeruginosa-induced NF-κB nuclear translocation. Oral inoculation via drinking water of IL-1R knockout mice resulted in higher rates of lung colonization and elevatedP. aeruginosa-specific antibody titers in a manner analogous to that of CFTR-deficient mice. Overall, rapid IL-1 release and signaling through IL-1R represent key steps in the innate immune response toP. aeruginosainfection, and this process is deficient in cells lacking functional CFTR.
Evidence of Immunostimulating Lipoprotein Existing in the Natural Lipoteichoic Acid Fraction
Authors: Hashimoto Masahito , Furuyashiki Maiko , Kaseya Ryoko , Fukada Yuka , Akimaru Mai , Aoyama Kazue , Okuno Toshiomi , Tamura Toshihide , Kirikae Teruo , Kirikae Fumiko , Eiraku Nobutaka , Morioka Hirofumi , Fujimoto Yukari , Fukase Koichi , Takashige Katsuhiro , Moriya Yoichiro , Kusumoto Shoichi , Suda Yasuo 
Published: February 2007

ABSTRACT

Lipoteichoic acid (LTA) is a cell surface glycoconjugate of gram-positive bacteria and is reported to activate the innate immune system. We previously reported that purified LTA obtained from
Enterococcus hirae
has no immunostimulating activity, but a subfraction (Eh-AF) in an LTA fraction possesses activity. In this study, we established a mouse monoclonal antibody neutralizing the activity of Eh-AF and investigated its inhibitory effects. Monoclonal antibody (MAbEh1) was established by the immunization of BALB/c mice with Eh-AF, followed by hybridoma screening based on its inhibitory effect for the production of interleukin-6 (IL-6) induced by Eh-AF. MAbEh1 neutralized the production of IL-6 by LTA fraction from not only
E. hirae
but also
Staphylococcus aureus
, while it failed to block that of lipopolysaccharide, suggesting that the antibody recognized a common active structure(s) in LTA fractions. Synthetic glycolipids in these LTAs did not induce cytokine production, at least in our system. Interestingly, the antibody was found to inhibit the activity of immunostimulating synthetic lipopeptides, Pam
3
CSK
4
and FSL-1. These results suggest that MAbEh1 neutralizes the activity of lipoprotein-like compounds which is responsible for the activity of the LTA fraction of
E. hirae
and
S. aureus
.
The Rollback of Democracy in Russia after Beslan
Authors: Lemaître Roemer 
Published: February 2007

AbstractThis contribution analyzes the political and legal changes implemented after "Russia's 9/11". President Putin used Beslan as eyewash to further increase his powers and to suppress or co-opt all independent sources of power in state and society. It is argued that several aspects of these reforms are in breach of the Russian Constitution and violate Russia's obligations under international (human rights) law. The contribution discusses the abolition of direct elections of regional leaders and the far-reaching amendments to the parliamentary election system in clear favor of the pro-Kremlin parties. It describes the growing state tutelage of civil society through the creation of a Public Chamber, the increased legal scrutiny of the activities of domestic and foreign NGOs as well as the formation of a loyal vanguard youth movement that could ultimately be deployed to ward off an "orange" revolution. Finally, it assesses the legality of new counterterrorism measures and briefly refers to the bottlenecks in the administration of justice unearthed by the first judgments of the European Court of Human Rights in cases stemming from Chechnya.
The Challenge of the Pentecostals in Asia Part One: Pentecostal Movements in Asia
Authors: Prior John Mansford 
Published: February 2007

AbstractIntroduction by the Managing Editor: John Mansford Prior SVD wrote an essay for the Asian Convention of the Pontifical Council for Culture planned for Jogyakarta, Indonesia, in June 12-17, 2006. The essay starts with a survey of the Pentecostal and charismatic movements in five Asian countries. Subsequently Prior reviews a growing awareness of 'sects and new religious movements' in church documents. Then he looks at how social science understands the 'rise of the sects' before he takes up the pastoral challenge to link the dynamism of Pentecostal/charismatic movements with the social conscience of basic ecclesial communities. The editing board of Exchange was impressed by the content of the essay and considered it to be of great importance to the readership of the journal. However, the essay was too long to be published in one issue. Therefore it is decided to divide it into parts. The first part gives the overview of Pentecostal and charismatic movements in Asia and the second part deals with the reaction of the Asian mainline churches, in particular the Roman Catholic Church. Part two will be published in the next issue.