bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of heavy silicone oil (Densiron‐68®) in the treatment of persistent macular holes
Authors: Lappas Alexandra , Heinrich Foerster Andreas Michael , Kirchhof Bernd 
Published: November 2008

Abstract.Purpose:  In this retrospective case series, we studied the effect of ‘heavy’ silicone oil on persisting macular holes. Patients with macular holes that failed to close after conventional macular hole surgery were retreated with the longterm internal tamponade Densiron‐68®.Methods:  Twelve patients with primary macular holes that persisted after pars plana vitrectomy, peeling of the internal limiting membrane and internal gas tamponade with SF6 (sulphur hexafluoride) were retreated with heavy silicone oil, Densiron‐68®, in the University Eye Hospital, Cologne. After 1.5–4 months the Densiron‐68® was removed. Best corrected visual acuity (VA), slit‐lamp examination, binocular fundus examination and optical coherence tomography (OCT) were used for evaluation pre‐ and postoperatively. The follow‐up period was 3–7 months.Results:  Preoperatively, all patients displayed full‐thickness macular holes, with a mean size of 502.25 μm (± 129.39 μm). Postoperatively, 11 of 12 macular holes were closed. One patient experienced a reopening of the macular hole. Mean VA was 20/250 (1.07 ± 0.22 logMAR) prior to treatment with Densiron‐68® and 20/160 (0.84 ± 0.24 logMAR) postoperatively. Visual acuity increased from baseline in nine patients and decreased in one.Conclusions:  Retreatment of persisting macular holes with the heavy, longterm tamponade Densiron‐68® resulted in anatomical closure of the hole in 11 of 12 cases. This result was accompanied by a functional improvement in VA in nine of 12 patients.
Investigation of Bartonella henselae in Cats in Ankara, Turkey
Authors: Celebi B. , Kilic S. , Aydin N. , Tarhan G. , Carhan A. , Babur C. 
Published: November 2008

SummaryThe purpose of this study was to determine Bartonella henselae prevalance in cats in Ankara. Whole bloods and sera collected from 256 cats were investigated for the presence feline Bartonella species by culture and sera were tested for the presence of antibodies against B. henselae IgG using immunofluorescence assay. Bartonella species were isolated by blood culture from 24 (9.4%) cats. Bartonella isolates were subjected to restriction fragment length polymorphism (RFLP) by using TaqI and HhaI endonucleases to identify species. Twenty‐one isolates were determined as B. henselae and three of 24 isolates were determined as Bartonella clarridgeiae with RFLP. The bacteraemia prevalence and seroprevalence of B. henselae IgG antibodies in cats was detected as 8.2% and 18.6% respectively. This is the first report on B. henselea and B. clarridgeiae in cats in Turkey.
Experimental Infection withToxocara catiin BALB/c Mice, Migratory Behaviour and Pathological Changes
Authors: Cardillo N. , Rosa A. , Ribicich M. , López C. , Sommerfelt I. 
Published: November 2008

SummaryExperimental inoculations of 1000Toxocara catilarval eggs were carried out in 18 BALB/c mice. TheT. catieggs used for inoculation were collected from the faeces of naturally infected cats. Euthanasia was performed on two mice on days 1, 2, 3, 4, 5, 6, 14, 21 and 28 post‐inoculation (p.i.). Tissue samples were taken for digestion and histopathology. Larvae were recovered from all infected mice and the average of all larvae recovered was 28.3% (95%; CI: 14.1–42.4). Maximum number was obtained from liver on days 1 and 2 p.i.; from the lung on day 2 p.i. and from the brain on day 28 p.i. In muscle, the recovery was high as from day 3 p.i., with the maximum obtained on day 28 p.i. Superficial foci of congestion and haemorrhage were macroscopically observed in the lungs between days 2 and 5 p.i. and in the brain between days 3 and 6 p.i. Microscopic lesions were observed in the liver between days 2 and 14 p.i., with periportal and subcapsule inflammatory infiltrates. In the lungs, haemorrhages and inflammatory infiltrates can be observed in the alveolar parenchyma, close to bronchioles and large blood vessels. In the brain, congestive areas without inflammatory reactions were seen. In muscle, the presence of inflammatory infiltrates and degenerated muscle can be observed surrounding a parasite larva. These same lesions were observed in myocardium and pericardium. The kidneys were congested with inflammatory infiltrates. The inflammatory cells present in all the tissues studied were lymphocytes, neutrophils and a few eosinophils. Formation of granulomas or signs of larva encapsulation were not observed. The migratory pattern ofT. catilarvae in BALB/c mice and its tendency to become concentrated in the muscle reinforce the importance of the mouse as a paratenic host for the parasite’s cycle in the environment.
Identification of Highly Specific and Cross‐Reactive Antigens of Leishmania Species by Antibodies from Leishmania (Leishmania) chagasi Naturally Infected Dogs
Authors: Vale A. M. , Fujiwara R. T. , Da Silva Neto A. F. , Miret J. A. , Alvarez D. C. C. , Da Silva J. C. F. , Campos‐Neto A. , Reed S. , Mayrink W. , Nascimento E. 
Published: November 2008

SummaryThe Leishmania species present a genetic homology that ranges from 69 to 90%. Because of this homology, heterologous antigens have been used in the immunodiagnosis and vaccine development against Leishmania infections. In the current work, we describe the identification of species‐specific and cross‐reactive antigens among several New World Leishmania species, using symptomatic and asymptomatic naturally Leishmania chagasi‐infected dog sera. Soluble antigens from five strains of New World Leishmania were separated by electrophoresis in SDS‐PAGE and immunoblotted. Different proteins were uniquely recognized in the L. chagasi panel by either symptomatic or asymptomatic dog sera suggesting their use as markers for the progression of disease and diagnosis of the initial (sub‐clinical) phase of the infection. Cross‐reactive antigens were identified using heterologous antigenic panels (L. amazonensis strains PH8 and BH6, L. guyanensis and L. braziliensis). L. guyanensis panel showed the highest cross‐reactivity against L. chagasi specific antibodies, suggesting that proteins from this extract might be suitable for the diagnosis of visceral canine leishmaniasis. Interestingly, the 51 and 97 kDa proteins of Leishmania were widely recognized (77.8% to 100%) among all antigenic panels tested, supporting their potential use for immunodiagnosis. Finally, we identified several leishmanial antigens that might be useful for routine diagnosis and seroepidemiological studies of the visceral canine leishmaniasis.
The Salmonella Enteritidis Lipopolysaccharide Biosynthesis Gene rfbH is Required for Survival in Egg Albumen
Authors: Gantois I. , Ducatelle R. , Pasmans F. , Haesebrouck F. , Van Immerseel F. 
Published: November 2008

Summary Salmonella Enteritidis is still a major cause of human food borne infections and can be associated with the consumption of meat and chicken eggs. It is the world’s most common cause of salmonellosis in part because it has the ability to colonize the oviduct and contaminate eggs. It was shown that when stored at room temperature, S. Enteritidis bacteria can multiply extensively in contaminated eggs. Using the in vivo expression technology, it was shown that the rfbH gene, involved in lipopolysaccharide O‐antigen synthesis, is transcriptionally induced during growth in whole eggs at room temperature. A S. Enteritidis ΔrfbH strain was unable to multiply in eggs at room temperature and did not survive in egg white at 42°C. The attenuation was most likely caused by an increased susceptibility of the ΔrfbH mutant to yet undefined antibacterial components of the egg albumen.
Sec- and Tat-Dependent Translocation of β-Lactamases across theEscherichia coliInner Membrane
Authors: Pradel N. , Delmas J. , Wu L. F. , Santini C. L. , Bonnet R. 
Published: November 2008

ABSTRACTβ-Lactamases represent the major resistance mechanism of gram-negative bacteria against β-lactam antibiotics. The amino acid sequences of these proteins vary widely, but all are located in the periplasm of bacteria. In this study, we investigated the translocation mechanism of representative β-lactamases in anEscherichia colimodel. N-terminal signal sequence analyses, antibiotic activity assay, and direct measurement of translocation of a green fluorescent protein (GFP) reporter fused to β-lactamases revealed that most were exported via the Sec pathway. However, theStenotrophomonas maltophiliaL2 β-lactamase was exported via theE. coliTat translocase, while theS. maltophiliaL1 β-lactamase was Sec dependent. These results show the possible Tat-dependent translocation of β-lactamases in theE. colimodel system. In addition, the mutation of the cytoskeleton-encoding genemreB, which may be involved in the spatial organization of penicillin-binding proteins, decreased the MIC of β-lactams for β-lactamase-producingE. coli. These findings provide new knowledge about β-lactamase translocation, a putative new target for addressing β-lactamase-mediated resistance.
Diverse Cytomegalovirus UL27 Mutations Adapt to Loss of Viral UL97 Kinase Activity under Maribavir
Authors: Chou Sunwen 
Published: November 2008

ABSTRACT
In vitro resistance to maribavir (MBV), a cytomegalovirus UL97 kinase inhibitor currently in clinical trials, is known to result from viral UL97 mutations that confer moderate to high-level resistance and UL27 mutations that confer low-level resistance. To add to the four reported UL27 mutations, cytomegalovirus isolates or strains were propagated under MBV. Four clinical isolates evolved UL27 mutations, which were first detected after 8 to 30 passages under drug selection. In three separate experiments, laboratory strain T2294, which contained an exonuclease mutation, developed UL27 mutations at 10 to 12 passages under MBV. Most of these isolates and strains also developed a UL97 mutation, commonly T409M, before or after the appearance of the UL27 mutation. The passage of two laboratory strains genetically defective in UL97, in the absence of MBV, likewise resulted in UL27 mutations. The nine UL27 mutations observed included multiple instances of point, stop, and frameshift mutations, which were individually transferred to a reference CMV strain and which were shown to confer two- to threefold increases in MBV inhibitory concentrations. In contrast, seven common UL27 amino acid changes found in baseline clinical isolates conferred no MBV resistance. The mutants with UL27 mutations had slightly attenuated growth. The frequent mutation of UL27 suggests that its normal expression is mildly disadvantageous to the virus in the absence of UL97 kinase activity, whether the latter results from MBV inhibition or a genetic defect. Although the function of UL27 is unknown, it does not appear to be a direct antiviral target for MBV.
Immunogenicity and Protective Efficacy of “
Mycobacterium w
” against
Mycobacterium tuberculosis
in Mice Immunized with Live versus Heat-Killed
M. w
by the Aerosol or Parenteral Route
Authors: Gupta Ankan , Geetha Nishamol , Mani Jiju , Upadhyay Pramod , Katoch V. M. , Natrajan M. , Gupta U. D. , Bhaskar Sangeeta 
Published: November 2008

ABSTRACT

As the disease caused by
Mycobacterium tuberculosis
continues to be a burden, there is a concerted effort to find new vaccines to combat this problem. One of the important vaccine strategies is whole bacterial vaccines. This approach relies on multiple antigens and built-in adjuvanticity. Other mycobacterial strains which share cross-reactive antigens with
M. tuberculosis
have been considered as alternatives to
M. bovis
for vaccine use. One such strain, “
Mycobacterium w
”, had been evaluated for its immunomodulatory properties in leprosy. A vaccine against leprosy based on killed
M. w
is approved for human use, where it has resulted in clinical improvement, accelerated bacterial clearance, and increased immune responses to
Mycobacterium leprae
antigens.
M. w
shares antigens not only with
M. leprae
but also with
M. tuberculosis
, and initial studies have shown that vaccination with killed
M. w
induces protection against tuberculosis in
Mycobacterium bovis
BCG responder, as well as BCG nonresponder, strains of mice. Hence, we further studied the protective potential of
M. w
and the underlying immune responses in the mouse model of tuberculosis. We analyzed the protective efficacy of
M. w
immunization in both live and killed forms through the parenteral route and by aerosol immunization, compared with that of BCG. Our findings provide evidence that
M. w
has potential protective efficacy against
M. tuberculosis. M. w
activates macrophage activity, as well as lymphocytes.
M. w
immunization by both the parenteral route and aerosol adminstration gives higher protection than BCG given by the parenteral route in the mouse model of tuberculosis.
Discriminating Virulence Mechanisms amongBacillus anthracisStrains by Using a Murine Subcutaneous Infection Model
Authors: Chand Hitendra S. , Drysdale Melissa , Lovchik Julie , Koehler Theresa M. , Lipscomb Mary F. , Lyons C. Rick 
Published: November 2008

ABSTRACTBacillus anthracisstrains harboring virulence plasmid pXO1 that encodes the toxin protein protective antigen (PA), lethal factor, and edema factor and virulence plasmid pXO2 that encodes capsule biosynthetic enzymes exhibit different levels of virulence in certain animal models. In the murine model of pulmonary infection,B. anthracisvirulence was capsule dependent but toxin independent. We examined the role of toxins in subcutaneous (s.c.) infections using two different genetically complete (pXO1+pXO2+) strains ofB. anthracis, strains Ames and UT500. Similar to findings for the pulmonary model, toxin was not required for infection by the Ames strain, because the 50% lethal dose (LD50) of a PA-deficient (PA−) Ames mutant was identical to that of the parent Ames strain. However, PA was required for efficient s.c. infection by the UT500 strain, because the s.c. LD50of a UT500 PA−mutant was 10,000-fold higher than the LD50of the parent UT500 strain. This difference between the Ames strain and the UT500 strain could not be attributed to differences in spore coat properties or the rate of germination, because s.c. inoculation with the capsulated bacillus forms also required toxin synthesis by the UT500 strain to cause lethal infection. The toxin-dependent phenotype of the UT500 strain was host phagocyte dependent, because eliminating Gr-1+phagocytes restored virulence to the UT500 PA−mutant. These experiments demonstrate that the dominant virulence factors used to establish infection byB. anthracisdepend on the route of inoculation and the bacterial strain.
The C-Type Lectin SIGNR1 BindsSchistosoma mansoniAntigens In Vitro, but SIGNR1-Deficient Mice Have Normal Responses during Schistosome Infection
Authors: Saunders Sean P. , Walsh Caitriona M. , Barlow Jillian L. , Mangan Niamh E. , Taylor Philip R. , McKenzie Andrew N. J. , Smith Philip , Fallon Padraic G. 
Published: November 2008

ABSTRACTThe de novo immune response to infectious organisms arises from the innate recognition of pathogen-associated molecular patterns (PAMPs) by the host's pattern recognition receptors (PRRs). As the generation of type 2 cytokine responses by the human trematode parasiteSchistosoma mansoniis glycan mediated, there is a particular potential role for a C-type lectin receptor (CLR) to mediate the innate recognition of schistosome PAMPs. One such CLR, dendritic cell-specific intracellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN; CD209), has been shown to recognize glycans expressed byS. mansonieggs. We show that SIGNR1 (SIGN-related 1; CD209b), a murine homologue of DC-SIGN that is expressed on macrophages, also binds both schistosome-soluble egg antigens and worm antigens in vitro. The generation of schistosome egg-induced pulmonary egg granulomas was not altered in SIGNR1-deficient mice. FollowingS. mansoniinfection, the SIGNR1-deficient mice had an unaltered phenotype with an intact immunological response and no difference in pathology. In this study we demonstrate that although SIGNR1 recognizesS. mansoniantigens in vitro, this CLR is redundant during infection. This study highlights the finding that although there was binding of SIGNR1 to immunogenic factors produced in theS. mansonilife cycle, this recognition does not translate to a functional in vivo role for the PRR during infection.
Sequential B-Cell Epitopes ofBacillus anthracisLethal Factor Bind Lethal Toxin-Neutralizing Antibodies
Authors: Nguyen Melissa L. , Crowe Sherry R. , Kurella Sridevi , Teryzan Simon , Cao Brian , Ballard Jimmy D. , James Judith A. , Farris A. Darise 
Published: November 2008

ABSTRACTThe bipartite anthrax lethal toxin (LeTx) consisting of protective antigen (PA) and lethal factor (LF) is a major virulence factor contributing to death from systemicBacillus anthracisinfection. The current vaccine elicits antibodies directed primarily to PA; however, in experimental settings serologic responses to LF can neutralize LeTx and contribute to protection against infection. The goals of the present study were to identify sequential B-cell epitopes of LF and to determine the capacity of these determinants to bind neutralizing antibodies. Sera of recombinant LF-immunized A/J mice exhibited high titers of immunoglobulin G anti-LF reactivity that neutralized LeTx in vitro 78 days after the final booster immunization and protected the mice from in vivo challenge with 3 50% lethal doses of LeTx. These sera bound multiple discontinuous epitopes, and there were major clusters of reactivity on native LF. Strikingly, all three neutralizing, LF-specific monoclonal antibodies tested bound specific peptide sequences that coincided with sequential epitopes identified in polyclonal antisera from recombinant LF-immunized mice. This study confirms that LF induces high-titer protective antibodies in vitro and in vivo. Moreover, the binding of short LF peptides by LF-specific neutralizing monoclonal antibodies suggests that generation of protective antibodies by peptide vaccination may be feasible for this antigen. This study paves the way for a more effective anthrax vaccine by identifying discontinuous peptide epitopes of LF.
Role of RpoS in the Virulence of
Citrobacter rodentium
Authors: Dong Tao , Coombes Brian K. , Schellhorn Herb E. 
Published: November 2008

ABSTRACT

Citrobacter rodentium
is a mouse enteropathogen that is closely related to
Escherichia coli
and causes severe colonic hyperplasia and bloody diarrhea.
C. rodentium
infection requires expression of genes of the locus of enterocyte effacement (LEE) pathogenicity island, which simulates infection by enteropathogenic
E. coli
and enterohemorrhagic
E. coli
in the human intestine, providing an effective model for studying enteropathogenesis. In this study we investigated the role of RpoS, the stationary phase sigma factor, in virulence in
C. rodentium
. Sequence analysis showed that the
rpoS
gene is highly conserved in
C. rodentium
and
E. coli
, exhibiting 92% identity. RpoS was critical for survival under heat shock conditions and during exposure to H
2
O
2
and positively regulated the expression of catalase KatE (HPII). The development of the RDAR (
r
ed
d
ry
a
nd
r
ough) morphotype, an important virulence trait in
E. coli
, was also mediated by RpoS in
C. rodentium
. Unlike
E. coli, C. rodentium
grew well in the mouse colon, and the wild-type strain colonized significantly better than
rpoS
mutants. However, a mutation in
rpoS
conferred a competitive growth advantage over the wild type both in vitro in Luria-Bertani medium and in vivo in the mouse colon. Survival analysis showed that the virulence of an
rpoS
mutant was attenuated. The expression of genes on the LEE pathogenicity island, which are essential for colonization and virulence, was reduced in the
rpoS
mutant. In conclusion, RpoS is important for the stress response and is required for full virulence in
C. rodentium
.
Direct and Indirect Impairment of Human Dendritic Cell Function by VirulentFrancisella tularensisSchu S4
Authors: Chase Jennifer C. , Celli Jean , Bosio Catharine M. 
Published: November 2008

ABSTRACTThe gram-negative, facultative intracellular bacteriumFrancisella tularensiscauses acute, lethal pneumonic disease following infection with only 10 CFU. The mechanisms used by the bacterium to accomplish this in humans are unknown. Here, we demonstrate that virulent, type AF. tularensisstrain Schu S4 efficiently infects and replicates in human myeloid dendritic cells (DCs). Despite exponential replication over time, Schu S4 failed to stimulate transforming growth factor β, interleukin-10 (IL-10), IL-6, IL-1β, IL-12, tumor necrosis factor alpha, alpha interferon (IFN-α), and IFN-β throughout the course of infection. Schu S4 also suppressed the ability of directly infected DCs to respond to different Toll-like receptor agonists. Furthermore, we also observed functional inhibition of uninfected bystander cells. This inhibition was mediated, in part, by a heat-stable bacterial component. Lipopolysaccharide (LPS) from Schu S4 was present in Schu S4-conditioned medium. However, Schu S4 LPS was weakly inflammatory and failed to induce suppression of DCs at concentrations below 10 μg/ml, and depletion of Schu S4 LPS did not significantly alleviate the inhibitory effect of Schu S4-conditioned medium in uninfected human DCs. Together, these data show that type AF. tularensisinterferes with the ability of a central cell type of the immune system, DCs, to alert the host of infection both intra- and extracellularly. This suggests that immune dysregulation byF. tularensisoperates on a broader and more comprehensive scale than previously appreciated.
β
2
-Microglobulin-Dependent Bacterial Clearance and Survival during Murine
Klebsiella pneumoniae
Bacteremia
Authors: Cogen Anna L. , Moore Thomas A. 
Published: November 2008

ABSTRACT

Klebsiella pneumoniae
is a leading cause of both community-acquired and nosocomial gram-negative bacterial pneumonia. A significant clinical complication of
Klebsiella
pulmonary infections is peripheral blood dissemination, resulting in a systemic infection concurrent with the localized pulmonary infection. We report here on the critical importance of β
2
-microglobulin expression during murine
K. pneumoniae
bacteremia. β
2
-Microglobulin knockout mice displayed significantly increased mortality upon intravenous inoculation that correlated with increased bacterial burden in the blood, liver, and spleen. As β
2
-microglobulin knockout mice lack both CD8
+
T cells and invariant NK T cells, mouse models specifically deficient in either cell population were examined to see if this would account for the increased mortality noted in β
2
-microglobulin knockout mice. Surprisingly, neither CD8 T-cell-deficient (TAP-1 knockout; in vivo anti-CD8 antibody treatment) nor invariant NK (iNK) T-cell-deficient (CD1d knockout, Jα281 knockout) mice were more susceptible to
K. pneumoniae
bacteremia. Combined, these studies clearly indicate the importance of a β
2
-microglobulin-dependent but CD8 T-cell- and iNK T-cell-independent mechanism critical for survival during
K. pneumoniae
bacteremia.