bluuebunny/crossref_metadata_2025_split huggingface dataset:
The O-Antigen Capsule of Salmonella enterica Serovar Typhimurium Facilitates Serum Resistance and Surface Expression of FliC
Authors: Marshall Joanna M. , Gunn John S. 
Published: July 2015

ABSTRACT

Group IV polysaccharide capsules are common in enteric bacteria and have more recently been described in nontyphoidal
Salmonella
species. Such capsules are known as O-antigen (O-Ag) capsules, due to their high degree of similarity to the O-Ag of the lipopolysaccharide (LPS
O-Ag
). Capsular polysaccharides are known virulence factors of many bacterial pathogens, facilitating evasion of immune recognition and systemic dissemination within the host. Previous studies on the O-Ag capsule of salmonellae have focused primarily on its role in bacterial surface attachment and chronic infection; however, the potential effects of the O-Ag capsule on acute pathogenesis have yet to be investigated. While much of the
in vivo
innate immune resistance of
Salmonella enterica
serovar Typhimurium is attributed to the high-molecular-weight LPS, we hypothesized that the O-Ag capsule may enhance this resistance by diminishing surface expression of pathogen-associated molecular patterns, such as flagella, and increasing resistance to host immune molecules. To test this hypothesis, O-Ag capsule-deficient mutants were constructed, and the loss of O-Ag capsular surface expression was confirmed through microscopy and immunoblotting. Loss of O-Ag capsule production did not alter bacterial growth or production of LPS. Western blot analysis and confocal microscopy revealed that O-Ag capsule-deficient mutants demonstrate reduced resistance to killing by human serum. Furthermore, O-Ag capsule-deficient mutants produced exclusively phase I flagellin (FliC). Although O-Ag capsule-deficient mutants did not exhibit reduced virulence in a murine model of acute infection,
in vitro
results indicate that the O-Ag capsule may function to modify the antigenic nature of the bacterial surface, warranting additional investigation of a potential role of the structure in pathogenesis.
Choriodecidual Group B Streptococcal Infection Induces miR-155-5p in the Fetal Lung in Macaca nemestrina
Authors: McAdams Ryan M. , Bierle Craig J. , Boldenow Erica , Weed Samantha , Tsai Jesse , Beyer Richard P. , MacDonald James W. , Bammler Theo K. , Liggitt H. Denny , Farin Federico M. , Vanderhoeven Jeroen , Rajagopal Lakshmi , Adams Waldorf Kristina M. 
Published: July 2015

ABSTRACT

The mechanisms underlying fetal lung injury remain poorly defined. MicroRNAs (miRNAs) are small noncoding, endogenous RNAs that regulate gene expression and have been implicated in the pathogenesis of lung disease. Using a nonhuman primate model of choriodecidual infection, we sought to determine if differentially expressed miRNAs were associated with acute fetal lung injury. After inoculating 10 chronically catheterized pregnant monkeys (
Macaca nemestrina
) with either group B streptococcus (GBS) at 1 × 10
6
CFU (
n
= 5) or saline (
n
= 5) in the choriodecidual space, we extracted fetal lung mRNA and miRNA and profiled the changes in expression by microarray analysis. We identified 9 differentially expressed miRNAs in GBS-exposed fetal lungs, but of these, only miR-155-5p was validated by quantitative reverse transcription-PCR (
P
= 0.02). Significantly elevated miR-155-5p expression was also observed when immortalized human fetal airway epithelial (FeAE) cells were exposed to proinflammatory cytokines (interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF-α]). Overexpression of miR-155-5p in FeAE cells in turn increased the production of IL-6 and CXCL10/gamma interferon-induced protein 10, which are implicated in leukocyte recruitment but also in protection from lung injury. Interestingly, while miR-155-5p decreased fibroblast growth factor 9 (FGF9) expression in a luciferase reporter assay, FGF9 levels were actually increased in GBS-exposed fetal lungs
in vivo
. FGF9 overexpression is associated with abnormal lung development. Thus, upregulation of miR-155-5p may serve as a compensatory mechanism to lessen the increase in FGF9 and prevent aberrant lung development. Understanding the complicated networks regulating lung development in the setting of infection is a key step in identifying how to prevent fetal lung injury leading to bronchopulmonary dysplasia.
The Legionella pneumophila Siderophore Legiobactin Is a Polycarboxylate That Is Identical in Structure to Rhizoferrin
Authors: Burnside Denise M. , Wu Yuyang , Shafaie Saman , Cianciotto Nicholas P. 
Published: July 2015

ABSTRACTLegionella pneumophila, the agent of Legionnaires' disease, secretes a siderophore (legiobactin) that promotes bacterial infection of the lung. In past work, we determined that cytoplasmic LbtA (fromLegiobactin geneA) promotes synthesis of legiobactin, inner membrane LbtB aids in export of the siderophore, and outer membrane LbtU and inner membrane LbtC help mediate ferrilegiobactin uptake and assimilation. However, the past studies examined legiobactin contained within bacterial culture supernatants. By utilizing high-pressure liquid chromatography that incorporates hydrophilic interaction-based chemistry, we have now purified legiobactin from supernatants of virulent strain 130b that is suitable for detailed chemical analysis. High-resolution mass spectrometry (MS) revealed that the molecular mass of (protonated) legiobactin is 437.140 Da. On the basis of the results obtained from both MS analysis and various forms of nuclear magnetic resonance, we found that legiobactin is composed of two citric acid residues linked by a putrescine bridge and thus is identical in structure to rhizoferrin, a polycarboxylate-type siderophore made by many fungi and several unrelated bacteria. Both purified legiobactin and rhizoferrin obtained from the fungusCunninghamella eleganswere able to promote Fe3+uptake by wild-typeL. pneumophilaas well as enhance growth of iron-starved bacteria. These results did not occur with 130b mutants lackinglbtUorlbtC, indicating that both endogenously made legiobactin and exogenously derived rhizoferrin are assimilated byL. pneumophilain an LbtU- and LbtC-dependent manner.
Candida albicans Quorum Sensing Molecules Stimulate Mouse Macrophage Migration
Authors: Hargarten Jessica C. , Moore Tyler C. , Petro Thomas M. , Nickerson Kenneth W. , Atkin Audrey L. 
Published: July 2015

ABSTRACTThe polymorphic commensal fungusCandida albicanscauses life-threatening disease via bloodstream and intra-abdominal infections in immunocompromised and transplant patients. Although host immune evasion is a common strategy used by successful human fungal pathogens,C. albicansprovokes recognition by host immune cells less capable of destroying it. To accomplish this,C. albicanswhite cells secrete a low-molecular-weight chemoattractive stimulant(s) of macrophages, a phagocyte that they are able to survive within and eventually escape from.C. albicansopaque cells do not secrete this chemoattractive stimulant(s). We report here a physiological mechanism that contributes to the differences in the interaction ofC. albicanswhite and opaque cells with macrophages.E,E-Farnesol, which is secreted by white cells only, is a potent stimulator of macrophage chemokinesis, whose activity is enhanced by yeast cell wall components and aromatic alcohols.E,E-farnesol results in up to an 8.5-fold increase in macrophage migrationin vitroand promotes a 3-fold increase in the peritoneal infiltration of macrophagesin vivo. Therefore, modulation of farnesol secretion to stimulate host immune recognition by macrophages may help explain why this commensal is such a successful pathogen.
The Poly-γ-d-Glutamic Acid Capsule Surrogate of the Bacillus anthracis Capsule Is a Novel Toll-Like Receptor 2 Agonist
Authors: Jeon Jun Ho , Lee Hae-Ri , Cho Min-Hee , Park Ok-Kyu , Park Jungchan , Rhie Gi-eun 
Published: July 2015

ABSTRACTBacillus anthracisis a pathogenic Gram-positive bacterium that causes a highly lethal infectious disease, anthrax. The poly-γ-d-glutamic acid (PGA) capsule is one of the major virulence factors ofB. anthracis, along with exotoxins. PGA enablesB. anthracisto escape phagocytosis and immune surveillance. Our previous study showed that PGA activates the human macrophage cell line THP-1 and human dendritic cells, resulting in the production of the proinflammatory cytokine interleukin-1β (IL-1β) (M. H. Cho et al., Infect Immun 78:387–392, 2010,http://dx.doi.org/10.1128/IAI.00956-09). Here, we investigated PGA-induced cytokine responses and related signaling pathways in mouse bone marrow-derived macrophages (BMDMs) usingBacillus licheniformisPGA as a surrogate forB. anthracisPGA. Upon exposure to PGA, BMDMs produced proinflammatory mediators, including tumor necrosis factor alpha (TNF-α), IL-6, IL-12p40, and monocyte chemoattractant protein 1 (MCP-1), in a concentration-dependent manner. PGA stimulated Toll-like receptor 2 (TLR2) but not TLR4 in Chinese hamster ovary cells expressing either TLR2 or TLR4. The ability of PGA to induce TNF-α and IL-6 was retained in TLR4−/−but not TLR2−/−BMDMs. Blocking experiments with specific neutralizing antibodies for TLR1, TLR6, and CD14 showed that TLR6 and CD14 also were necessary for PGA-induced inflammatory responses. Furthermore, PGA enhanced activation of mitogen-activated protein (MAP) kinases and nuclear factor-kappa B (NF-κB), which are responsible for expression of proinflammatory cytokines. Additionally, PGA-induced TNF-α production was abrogated not only in MyD88−/−BMDMs but also in BMDMs pretreated with inhibitors of MAP kinases and NF-κB. These results suggest that immune responses induced by PGA occur via TLR2, TLR6, CD14, and MyD88 through activation of MAP kinase and NF-κB pathways.
RecF and RecR Play Critical Roles in the Homologous Recombination and Single-Strand Annealing Pathways of Mycobacteria
Authors: Gupta Richa , Shuman Stewart , Glickman Michael S. 
Published: July 2015

ABSTRACT

Mycobacteria encode three DNA double-strand break repair pathways: (i) RecA-dependent homologous recombination (HR), (ii) Ku-dependent nonhomologous end joining (NHEJ), and (iii) RecBCD-dependent single-strand annealing (SSA). Mycobacterial HR has two presynaptic pathway options that rely on the helicase-nuclease AdnAB and the strand annealing protein RecO, respectively. Ablation of
adnAB
or
recO
individually causes partial impairment of HR, but loss of
adnAB
and
recO
in combination abolishes HR. RecO, which can accelerate annealing of single-stranded DNA
in vitro
, also participates in the SSA pathway. The functions of RecF and RecR, which, in other model bacteria, function in concert with RecO as mediators of RecA loading, have not been examined in mycobacteria. Here, we present a genetic analysis of
recF
and
recR
in mycobacterial recombination. We find that RecF, like RecO, participates in the AdnAB-independent arm of the HR pathway and in SSA. In contrast, RecR is required for all HR in mycobacteria and for SSA. The essentiality of RecR as an agent of HR is yet another distinctive feature of mycobacterial DNA repair.

IMPORTANCE
This study clarifies the molecular requirements for homologous recombination in mycobacteria. Specifically, we demonstrate that RecF and RecR play important roles in both the RecA-dependent homologous recombination and RecA-independent single-strand annealing pathways. Coupled with our previous findings (R. Gupta, M. Ryzhikov, O. Koroleva, M. Unciuleac, S. Shuman, S. Korolev, and M. S. Glickman, Nucleic Acids Res 41:2284–2295, 2013,
http://dx.doi.org/10.1093/nar/gks1298
), these results revise our view of mycobacterial recombination and place the RecFOR system in a central position in homology-dependent DNA repair.
Function of the Histone-Like Protein H-NS in Motility of Escherichia coli: Multiple Regulatory Roles Rather than Direct Action at the Flagellar Motor
Authors: Kim Eun A , Blair David F. 
Published: July 2015

ABSTRACT

A number of investigations of
Escherichia coli
have suggested that the DNA-binding protein H-NS, in addition to its well-known functions in chromosome organization and gene regulation, interacts directly with the flagellar motor to modulate its function. Here, in a study initially aimed at characterizing the H-NS/motor interaction further, we identify problems and limitations in the previous work that substantially weaken the case for a direct H-NS/motor interaction. Null
hns
mutants are immotile, largely owing to the downregulation of the flagellar master regulators FlhD and FlhC. We, and others, previously reported that an
hns
mutant remains poorly motile even when FlhDC are expressed constitutively. In the present work, we use better-engineered strains to show that the motility defect in a Δ
hns
, FlhDC-constitutive strain is milder than that reported previously and does not point to a direct action of H-NS at the motor. H-NS regulates numerous genes and might influence motility via a number of regulatory molecules besides FlhDC. To examine the sources of the motility defect that persists in an FlhDC-constitutive Δ
hns
mutant, we measured transcript levels and overexpression effects of a number of genes in candidate regulatory pathways. The results indicate that H-NS influences motility via multiple regulatory linkages that include, minimally, the messenger molecule cyclic di-GMP, the biofilm regulatory protein CsgD, and the sigma factors σ
S
and σ
F
. The results are in accordance with the more standard view of H-NS as a regulator of gene expression rather than a direct modulator of flagellar motor performance.

IMPORTANCE
Data from a number of previous studies have been taken to indicate that the nucleoid-organizing protein H-NS influences motility not only by its well-known DNA-based mechanisms but also by binding directly to the flagellar motor to alter function. In this study, H-NS is shown to influence motility through diverse regulatory pathways, but a direct interaction with the motor is not supported. Previous indications of a direct action at the motor appear to be related to the use of nonnull strains and, in some cases, a failure to effectively bypass the requirement for H-NS in the expression of the flagellar regulon. These findings call for a substantially revised interpretation of the literature concerning H-NS and flagellar motility and highlight the importance of H-NS in diverse regulatory processes involved in the motile-sessile transition.
Lessons in Fundamental Mechanisms and Diverse Adaptations from the 2015 Bacterial Locomotion and Signal Transduction Meeting
Authors: Prüβ Birgit M. , Liu Jun , Higgs Penelope I. , Thompson Lynmarie K. 
Published: July 2015

ABSTRACT
In response to rapid changes in their environment, bacteria control a number of processes, including motility, cell division, biofilm formation, and virulence. Research presented in January 2015 at the biennial Bacterial Locomotion and Signal Transduction (BLAST) meeting in Tucson, AZ, illustrates the elegant complexity of the nanoarrays, nanomachines, and networks of interacting proteins that mediate such processes. Studies employing an array of biophysical, genetic, cell biology, and mathematical methods are providing an increasingly detailed understanding of the mechanisms of these systems within well-studied bacteria. Furthermore, comparisons of these processes in diverse bacterial species are providing insight into novel regulatory and functional mechanisms. This review summarizes research presented at the BLAST meeting on these fundamental mechanisms and diverse adaptations, including findings of importance for applications involving bacteria of medical or agricultural relevance.
Injury risk is low among world-class volleyball players: 4-year data from the FIVB Injury Surveillance System
Authors: Bere Tone , Kruczynski Jacek , Veintimilla Nadège , Hamu Yuichiro , Bahr Roald 
Published: July 2015

BackgroundLittle is known about the rate and pattern of injuries in international volleyball competition.ObjectiveTo describe the risk and pattern of injuries among world-class players based on data from the The International Volleyball Federation (FIVB) Injury Surveillance System (ISS) (junior and senior, male and female).MethodsThe FIVB ISS is based on prospective registration of injuries by team medical staff during all major FIVB tournaments (World Championships, World Cup, World Grand Prix, World League, Olympic Games). This paper is based on 4-year data (September 2010 to November 2014) obtained through the FIVB ISS during 32 major FIVB events (23 senior and 9 junior).ResultsThe incidence of time-loss injuries during match play was 3.8/1000 player hours (95% CI 3.0 to 4.5); this was greater for senior players than for junior players (relative risk: 2.04, 1.29 to 3.21), while there was no difference between males and females (1.04, 0.70 to 1.55). Across all age and sex groups, the ankle was the most commonly injured body part (25.9%), followed by the knee (15.2%), fingers/thumb (10.7%) and lower back (8.9%). Injury incidence was greater for centre players and lower for liberos than for other player functions; injury patterns also differed between player functions.ConclusionsVolleyball is a very safe sport, even at the highest levels of play. Preventive measures should focus on acute ankle and finger sprains, and overuse injuries in the knee, lower back and shoulder.
Mitosin and pHH3 predict poorer survival in astrocytomas WHO grades II and III
Authors: Varughese R K , Lind-Landström T , Habberstad A H , Salvesen Ø , Haug C S , Sundstrøm S , Torp S H 
Published: July 2015

Aims:The limitations of the current WHO classification of astrocytomas call for a sustained effort to improve diagnostic and prognostic accuracy. The relationship between tumour growth and clinical outcome suggests that proliferative activity should be examined. The objective of this study was to evaluate the diagnostic and prognostic value of the proliferation markers mitosin and phosphohistone H3 (pHH3) in infiltrative astrocytomas WHO grades II and III and compare the findings with mitotic count and Ki-67/MiB-1 immunostaining.Methods:Fifty-nine and thirty-three infiltrative astrocytomas WHO grades II and III, respectively, were immunostained with the proliferation markers mitosin and pHH3 using standard immunohistochemical procedures. The expression was quantified as a proliferative index (PI) and statistically evaluated with Spearman's rank correlation test, Wilcoxon-Mann-Whitney U test, and univariable and multivariable COX regression survival analyses.Results:Significant positive correlations were found between these proliferation markers. The number of mitoses, pHH3 mitotic figures (MFs), the Ki-67/MiB-1 PI and the mitosin PI were greater in WHOgrade III anaplastic astrocytomas compared to WHO grade II diffuse astrocytomas, while pHH3 PI only showed a trend. All proliferation markers were associated with poorer prognosis, but mitotic count was not. Ki-67/MiB-1, mitosin and pHH3 MF achieved statistical significance in the univariable analyses of both time to relapse (TTR) and overall survival (OS). Only mitosin remained significant in both multivariable analyses. pHH3 was significant in the multivariable analysis of OS but not of TTR. Clinical factors including age, extent of surgical resection and WHO performance status were also significantly correlated with survival.Conclusions:In conclusion, mitosin and pHH3 immunostaining have prognostic and diagnostic value in the clinical assessment of patients with infiltrative astrocytomas. The inclusion of proliferation markers in a layered diagnosis should be considered in the upcoming revision of the WHO classification system.
Path integral for spinning particle subjected to the constant electromagnetic field
Authors: Merdaci A. , Boudiaf N. , Chetouani L. 
Published: July 2015

The problem of the Dirac particle submitted to a wave [Formula: see text] of a four-dimensional constant electromagnetic tensor is solved with the path integral approach via the use of Lorentz transformation and with an adequate choice for the velocity of the mobile referential.We show that the supersymmetric action associated to the pair [Formula: see text] can be determined from that associated to the pair [Formula: see text] and from that associated to the pair [Formula: see text] following simple relations.The wave functions and the energy spectrums are thus exactly determined and tested. Special cases are considered as well.
Talas–Fergana Fault Cenozoic timing of deformation and its relation to Pamir indentation
Authors: Bande Alejandro , Sobel Edward R. , Mikolaichuk Alexander , Torres Acosta Verónica 
Published: July 2015

Abstract

Regional strike-slip faults are widely distributed in continental interiors and play a major role in the distribution of far-field deformation due to continental collisions. Constraining the deformation history of the Talas–Fergana Fault (TFF), one of the largest of such faults in the Himalayan deformed interior, is vital to comprehend the hinterland kinematics of the India–Asia collision. New apatite fission track results from the NW Tien Shan define a rapid exhumation event at
c.
25 Ma. This event is correlated with a synchronous pulse in the South Tien Shan, implying that both ranges experienced a simultaneous onset of rapid exhumation. We suggest that strike-slip motion along the TFF commenced at
c.
25 Ma, facilitating counter-clockwise rotation of the Fergana Basin and enabling exhumation of the linked horsetail splays. Pamir indentation, located south of the Western Tien Shan, is postulated to be underway by
c.
20 Ma. Recently published results suggest synchronous strike-slip deformation in the western Tarim Basin and eastern flank of the Pamir. Based on our results and published data, we are able to connect Tarim and Pamir deformation to the onset of TFF slip. We suggest that this pre-existing regional structure was responsible for transferring Pamir-induced shortening to the NW Tien Shan.

Supplementary material:
Supplementary material is available at
http://www.geolsoc.org.uk/SUP18845
Inelastic Neutron Scattering Studies on the Crystal Field Excitations in Superconducting NdFeAsO0.85F0.15
Authors: Cheng Peng , Bao Wei , Danilkin Sergey , Zhao Tiesong , Sheng Jieming , Liu Juanjuan , Luo Wei , Wang Jinchen 
Published: July 2015

Inelastic neutron scattering experiments were performed on polycrystalline samples of NdFeAsO0.85F0.15over a wide temperature range (3 K–250 K). Based on the analysis of the experimental data, a Nd3+CF energy level scheme is proposed to give a consistent explanation about the observed CF transitions. The observed extra ground-state CF transitions could not be simply explained by the transitions between five Kramers doublets split from the Nd3+   4I9/2ground state in theC4vpoint symmetry. A reliable explanation would be a superposition of crystal fields due to different local symmetries around the Nd3+ions induced by the fluorine doping.