bluuebunny/crossref_metadata_2025_split huggingface dataset:
Amino Acid Substitutions in GyrA ofBurkholderia glumaeAre Implicated in Not Only Oxolinic Acid Resistance but Also Fitness on Rice Plants
Authors: Maeda Yukiko , Kiba Akinori , Ohnishi Kouhei , Hikichi Yasufumi 
Published: December 2006

ABSTRACTOxolinic acid (OA) resistance in field isolates ofBurkholderia glumae, a causal agent of bacterial grain rot, is dependent on an amino acid substitution at position 83 in GyrA (GyrA83). In the present study, among spontaneous in vitro mutants from the OA-sensitiveB. glumaestrain Pg-10, we selected OA-resistant mutants that emerged at a rate of 5.7 × 10−10. Nucleotide sequence analysis of the quinolone resistance-determining region in GyrA showed that Gly81Cys, Gly81Asp, Asp82Gly, Ser83Arg, Asp87Gly, and Asp87Asn are observed in these OA-resistant mutants. The introduction of each amino acid substitution into Pg-10 resulted in OA resistance, similar to what was observed for mutants with the responsible amino acid substitution. In vitro growth of recombinants with Asp82Gly was delayed significantly compared to that of Pg-10; however, that of the other recombinants did not differ significantly. The inoculation of each recombinant into rice spikelets did not result in disease. In inoculated rice spikelets, recombinants with Ser83Arg grew less than Pg-10 during flowering, and growth of the other recombinants was reduced significantly. On the other hand, the reduced growth of recombinants with Ser83Arg in spikelets was compensated for under OA treatment, resulting in disease. These results suggest that amino acid substitutions in GyrA ofB. glumaeare implicated in not only OA resistance but also fitness on rice plants. Therefore, GyrA83 substitution is thought to be responsible for OA resistance inB. glumaefield isolates.
Identification of the Mycobacterial Subcomponents Involved in the Release of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand from Human Neutrophils
Authors: Simons Mark P. , Moore Jill M. , Kemp Troy J. , Griffith Thomas S. 
Published: December 2006

ABSTRACTIntravesical administration ofMycobacterium bovisbacillus Calmette-Guérin (BCG) continues to be a successful immunotherapy for superficial bladder cancer. Recently, workers in our laboratory observed expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) on neutrophils in voided urine following BCG therapy. Neutrophils released a soluble and functional form of TRAIL when they were stimulated in vitro with BCG, and the activity was localized predominantly to the cell wall fraction. In this study, we examined the ability of individual mycobacterial components to stimulate TRAIL release from neutrophils. Our results demonstrated that cell wall-derived lipoarabinomannan (LAM), mycolyl arabinogalactan-peptidoglycan complex, and a Triton X-114 (Tx114)-solubilized protein pool were effective agonists of TRAIL release from neutrophils. Mycobacterial DNA was also an agonist of TRAIL release from neutrophils. Furthermore, purified antigen 85 ABC complex and alpha-crystallin (HspX), two major cell wall antigens present in the Tx114 pool, induced TRAIL release from neutrophils. The Tx114 pool stimulated HEK-293 cells expressing either Toll-like receptor 2/1 (TLR2/1) or TLR2/6, but only HspX was able to stimulate TLR2/6-expressing cells. TLR4/MD2/CD14-expressing cells responded only to LAM. Collectively, these results suggested that TRAIL release from neutrophils was induced through the recognition of multiple mycobacterial components by TLR2 and TLR4.
A MyD88-Deficient Mouse Model Reveals a Role for Nramp1 in
Campylobacter jejuni
Infection
Authors: Watson Robert O. , Novik Veronica , Hofreuter Dirk , Lara-Tejero María , Galán Jorge E. 
Published: December 2006

ABSTRACT

Campylobacter jejuni
is a major worldwide cause of enteric illnesses. Adult immunocompetent mice are not susceptible to
C. jejuni
infection. However, we show here that mice deficient in the adaptor protein myeloid differentiation factor 88 (MyD88), which is required for signaling through most Toll-like receptors, can be stably colonized by
C. jejuni
but not by isogenic derivatives carrying mutations in known virulence genes. We also found that Nramp1 deficiency increases the mouse susceptibility to
C. jejuni
infection when administered systemically. These results indicate that MyD88-deficient mice could be a useful model to study
C. jejuni
colonization and reveal a potential role for Nramp1 in the control of this bacterial pathogen.
“
Candidatus
Helicobacter heilmannii” from a Cynomolgus Monkey Induces Gastric Mucosa-Associated Lymphoid Tissue Lymphomas in C57BL/6 Mice
Authors: Nakamura Masahiko , Murayama Somay Yamagata , Serizawa Hiroshi , Sekiya Yukie , Eguchi Masahiro , Takahashi Shinichi , Nishikawa Kaori , Takahashi Tetsufumi , Matsumoto Tsukasa , Yamada Haruki , Hibi Toshifumi , Tsuchimoto Kanji , Matsui Hidenori 
Published: December 2006

ABSTRACT

Both
Helicobacter pylori
and “
Candidatus
Helicobacter heilmannii” infections are associated with peptic ulcers, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphomas. However, good animal models of
H. pylori
clinical diseases are rare. In this study, we aimed to establish an animal model of “
Candidatus
Helicobacter heilmannii” gastric MALT lymphoma. We used a urease-positive gastric mucosal and mucus homogenate from a cynomolgus monkey maintained in C57BL/6 mouse stomachs. The bacterium in the homogenate was identified as “
Candidatus
Helicobacter heilmannii” based on a DNA sequence analysis of the 16S rRNA and urease genes. Mucosal and mucus homogenates were used to inoculate C57BL/6 mice, which were then examined for 24 months. We observed a gradual increase in the surface area of protrusive lesions in almost all infected C57BL/6 mouse fundic stomachs 6 months after infection. Light microscopic observations revealed an accumulation of B lymphocytes along with destruction of glandular elements and the presence of lymphoepithelial lesions consistent with low-grade MALT lymphomas. Electron microscopic observation revealed numerous “
Candidatus
Helicobacter heilmannii” bacilli in the fundic glandular lumen, the intracellular canaliculi, and the cytoplasm of intact cells, as well as damaged parietal cells. In conclusion, “
Candidatus
Helicobacter heilmannii” induced gastric MALT lymphomas in almost 100% of infected C57BL/6 mice after a 6-month period associated with the destruction of parietal cells.
Analysis of the Polysaccharide Capsule of the Systemic Pathogen
Streptococcus iniae
and Its Implications in Virulence
Authors: Lowe Beth A. , Miller Jesse D. , Neely Melody N. 
Published: December 2006

ABSTRACT

Systemic pathogens have developed numerous strategies for evading the defenses of the host, permitting dissemination and multiplication in various tissues. One means of survival in the host, particularly in the bloodstream, has been attributed to the ability to avoid phagocytosis via capsular polysaccharide. To further define the virulence capacity of
Streptococcus iniae
, a zoonotic pathogen with the ability to cause severe systemic disease in both fish and humans, we performed an analysis of the capsule locus. The initial analysis included cloning and sequencing of the capsule synthesis operon, which revealed an approximately 21-kb region that is highly homologous to capsule operons of other streptococci. A genetic comparison of
S. iniae
virulent strain 9117 and commensal strain 9066 revealed that the commensal strain does not have the central region of the capsule operon composed of several important capsule synthesis genes. Four 9117 insertion or deletion mutants with mutations in the beginning, middle, or end of the capsule locus were analyzed to determine their capsule production and virulence. Virulence profiles were analyzed for each mutant using three separate criteria, which demonstrated the attenuation of each mutant in several tissue environments. These analyses also provided insight into the different responses of the host to each mutant strain compared to a wild-type infection. Our results demonstrate that capsule is not required for all host environments, while excess capsule is also not optimal, suggesting that for an “ideal” systemic infection, capsule production is most likely regulated while the bacterium is in different environments of the host.
Simultaneous Induction of Apoptotic and Survival Signaling Pathways in Macrophage-Like THP-1 Cells by Shiga Toxin 1
Authors: Lee Sang-Yun , Cherla Rama P. , Tesh Vernon L. 
Published: December 2006

ABSTRACT

Shiga toxins have been shown to induce apoptosis in many cell types. However, Shiga toxin 1 (Stx1) induced only limited apoptosis of macrophage-like THP-1 cells in vitro. The mechanisms regulating macrophage death or survival following toxin challenge are unknown. Differentiated THP-1 cells expressed tumor necrosis factor receptors and membrane-associated tumor necrosis factor alpha (TNF-α) and produced soluble TNF-α after exposure to Stx1. However, the cells were refractory to apoptosis induced by TNF-α, although the cytokine modestly increased apoptosis in the presence of Stx1. Despite the partial resistance of macrophage-like THP-1 cells to Stx1-mediated killing, treatment of these cells with Stx1 activated a broad array of caspases, disrupted the mitochondrial membrane potential (ΔΨ
m
), and released cytochrome
c
into the cytoplasm. The ΔΨ
m
values were greatest in cells that had detached from plastic surfaces. Specific caspase inhibitors revealed that caspase-3, caspase-6, caspase-8, and caspase-9 were primarily involved in apoptosis induction. The antiapoptotic factors involved in macrophage survival following toxin challenge include inhibitors of apoptosis proteins and X-linked inhibitor of apoptosis protein. NF-κB and JNK mitogen-activated protein kinases (MAPKs) appeared to activate survival pathways, while p38 MAPK was involved in proapoptotic signaling. The JNK and p38 MAPKs were shown to be upstream signaling pathways which may regulate caspase activation. Finally, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK and p38 MAPK activation, while macrophage-like cells treated with cycloheximide remained viable and showed transient activation of MAPKs. Collectively, these data suggest that Stx1 activates both apoptotic and cell survival signaling pathways in macrophage-like THP-1 cells.
Helicobacter pylori
CagA Induces AGS Cell Elongation through a Cell Retraction Defect That Is Independent of Cdc42, Rac1, and Arp2/3
Authors: Bourzac Kevin M. , Botham Crystal M. , Guillemin Karen 
Published: December 2006

ABSTRACT

Helicobacter pylori
, which infects over one-half the world's population, is a significant risk factor in a spectrum of gastric diseases, including peptic ulcers and gastric cancer. Strains of
H. pylori
that deliver the effector molecule CagA into host cells via a type IV secretion system are associated with more severe disease outcomes. In a tissue culture model of infection, CagA delivery results in a dramatic cellular elongation referred to as the “hummingbird” phenotype, which is characterized by long, thin cellular extensions. These actin-based cytoskeletal rearrangements are reminiscent of structures that are regulated by Rho GTPases and the Arp2/3 complex. We tested whether these signaling pathways were important in the
H. pylori
-induced cell elongation phenotype. Contrary to our expectations, we found that these molecules are dispensable for cell elongation. Instead, time-lapse video microscopy revealed that cells infected by
cagA
+
H. pylori
become elongated because they fail to release their back ends during cell locomotion. Consistent with a model in which CagA causes cell elongation by inhibiting the disassembly of adhesive cell contacts at migrating cells' lagging ends, immunohistochemical analysis revealed that focal adhesion complexes persist at the distal tips of elongated cell projections. Thus, our data implicate a set of signaling molecules in the hummingbird phenotype that are different than the molecules previously suspected.
Extensive and Genome-Wide Changes in the Transcription Profile ofStaphylococcus aureusInduced by Modulating the Transcription of the Cell Wall Synthesis GenemurF
Authors: Sobral Rita G. , Jones Alison E. , Des Etages Shelley G. , Dougherty Thomas J. , Peitzsch Robert M. , Gaasterland Terry , Ludovice Ana Madalena , de Lencastre Hermínia , Tomasz Alexander 
Published: December 2006

ABSTRACTAmurFconditional mutant was used to evaluate the effect of suboptimal transcription of this gene on the transcriptome of the methicillin-resistantStaphylococcus aureusstrain COL. The mutant was grown in the presence of optimal and suboptimal concentrations of the inducer, and the relative levels of transcription of genes were evaluated genome wide with an Affymetrix DNA microarray that included all open reading frames (ORFs) as well as intergenic sequences derived from four sequencedS. aureusstrains. Using a sensitivity threshold value of 1.5, suboptimal expression ofmurFaltered the transcription of a surprisingly large number of genes, i.e., 668 out of the 2,740 ORFs (close to one-fourth of all ORFs), of the genome ofS. aureusstrain COL. The genes with altered transcription were distributed evenly around theS. aureuschromosome, and groups of genes involved with distinct metabolic functions responded in unique and operon-specific manners to modulation inmurFtranscription. For instance, all genes belonging to theisdoperon and all but 2 of the 35 genes of prophage L54a were down-regulated, whereas all but one of the 21 members of thevraSRregulon and most of the 79 virulence-related genes (those for fibronectin binding proteins A and B, clumping factor A, gamma hemolysin, enterotoxin B, etc.) were up-regulated in cells with suboptimal expression ofmurF. Most importantly, the majority of these altered gene expression profiles were reversible by resupplying the optimal concentration of IPTG (isopropyl-β-d-thiogalactopyranoside) to the culture. The observations suggest the coordinate regulation of a large sector of theS. aureustranscriptome in response to a disturbance in cell wall synthesis.
Characterization of Changes to the Cell Surface during the Life Cycle of
Streptomyces coelicolor
: Atomic Force Microscopy of Living Cells
Authors: Del Sol Ricardo , Armstrong Ian , Wright Chris , Dyson Paul 
Published: December 2006

ABSTRACT

Cell surface changes that accompany the complex life cycle of
Streptomyces coelicolor
were monitored by atomic force microscopy (AFM) of living cells. Images were obtained using tapping mode to reveal that young, branching vegetative hyphae have a relatively smooth surface and are attached to an inert silica surface by means of a secreted extracellular matrix. Older hyphae, representing a transition between substrate and aerial growth, are sparsely decorated with fibers. Previously, a well-organized stable mosaic of fibers, called the rodlet layer, coating the surface of spores has been observed using electron microscopy. AFM revealed that aerial hyphae, prior to sporulation, possess a relatively unstable dense heterogeneous fibrous layer. Material from this layer is shed as the hyphae mature, revealing a more tightly organized fibrous mosaic layer typical of spores. The aerial hyphae are also characterized by the absence of the secreted extracellular matrix. The formation of sporulation septa is accompanied by modification to the surface layer, which undergoes localized temporary disruption at the sites of cell division. The characteristics of the hyphal surfaces of mutants show how various chaplin and rodlin proteins contribute to the formation of fibrous layers of differing stabilities. Finally, older spores with a compact rodlet layer develop surface concavities that are attributed to a reduction of intracellular turgor pressure as metabolic activity slows.
Transposon Tn
7
Is Widespread in Diverse Bacteria and Forms Genomic Islands
Authors: Parks Adam R. , Peters Joseph E. 
Published: December 2006

ABSTRACT

We find that relatives of the bacterial transposon Tn
7
are widespread in disparate environments and phylogenetically diverse species. These elements form functionally diverse genomic islands at the specific site of Tn
7
insertion adjacent to
glmS
. This work presents the first example of genomic island formation by a DDE type transposon.
Colony Spreading in
Staphylococcus aureus
Authors: Kaito Chikara , Sekimizu Kazuhisa 
Published: December 2006

ABSTRACT

Wild-type
Staphylococcus aureus
rapidly expands on the surface of soft agar plates. The rates of expansion and the shapes of the resultant giant colonies were distinct for different strains of laboratory stocks and clinical isolates. The colony spreading abilities did not correlate with the biofilm-forming abilities in these strains. Insertional disruption of the
dltABCD
operon, which functions at the step of
d
-alanine addition to teichoic acids, and of the
tagO
gene, which is responsible for the synthesis of wall teichoic acids, decreased the colony spreading ability. The results indicate that wall teichoic acids and
d
-alanylation of teichoic acids are required for colony spreading.
Effects of Phenotype and Genotype on Methods for Detection of Extended-Spectrum-β-Lactamase-Producing Clinical Isolates ofEscherichia coliandKlebsiella pneumoniaein Norway
Authors: Tofteland Ståle , Haldorsen Bjørg , Dahl Kristin H. , Simonsen Gunnar S. , Steinbakk Martin , Walsh Timothy R. , Sundsfjord Arnfinn ,   the Norwegian ESBL Study Group
Published: December 2006

ABSTRACTConsecutive clinical isolates ofEscherichia coli(n= 87) andKlebsiella pneumoniae(n= 25) with reduced susceptibilities to oxyimino-cephalosporins (MICs > 1 mg/liter) from 18 Norwegian laboratories during March through October 2003 were examined forblaTEM/SHV/CTX-Mextended-spectrum-β-lactamase (ESBL) genes, oxyimino-cephalosporin MIC profiles, ESBL phenotypes (determined by the ESBL Etest and the combined disk and double-disk synergy [DDS] methods), and susceptibility to non-β-lactam antibiotics. Multidrug-resistant CTX-M-15-like (n= 23) and CTX-M-9-like (n= 15) ESBLs dominated among the 50 ESBL-positiveE. coliisolates. SHV-5-like (n= 9) and SHV-2-like (n= 4) ESBLs were the most prevalent in 19 ESBL-positiveK. pneumoniaeisolates. Discrepant ESBL phenotype test results were observed for one major (CTX-M-9) and several minor (TEM-128 and SHV-2/-28) ESBL groups and in SHV-1/-11-hyperproducing isolates. Negative or borderline ESBL results were observed when low-MIC oxyimino-cephalosporin substrates were used to detect clavulanic acid (CLA) synergy. CLA synergy was detected by the ESBL Etest and the DDS method but not by the combined disk method in SHV-1/-11-hyperproducing strains. The DDS method revealed unexplained CLA synergy in combination with aztreonam and cefpirome in threeE. colistrains. The relatively high proportion of ESBL-producingE. coliorganisms with a low ceftazidime MIC in Norway emphasizes that cefpodoxime alone or both cefotaxime and ceftazidime should be used as substrates for ESBL detection.
Laribacter hongkongensis
Isolated from a Patient with Community-Acquired Gastroenteritis in Hangzhou City
Authors: Ni Xiao-Ping , Ren Shu-Hua , Sun Jian-Rong , Xiang Hai-Qing , Gao Yan , Kong Qing-Xin , Cha Jie , Pan Jing-Chao , Yu Hua , Li Hua-Ming 
Published: December 2006

ABSTRACT

We describe the isolation of
Laribacter hongkongensis
in Hangzhou City, People's Republic of China. One strain of bacterium, named LHHZ242, had many of the same phenotypic and genotypic characteristics as
Laribacter hongkongensis
described in previous publications. This discovery proves that
Laribacter hongkongensis
is also associated with community-acquired gastroenteritis outside Hong Kong.
Comparison of Serological Test Kits for Diagnosis of Typhoid Fever in the Philippines
Authors: Kawano Razel L. , Leano Susan A. , Agdamag Dorothy May A. 
Published: December 2006

ABSTRACT

We evaluated four recent antibody-detection kits for typhoid fever by using 177 febrile patients from our hospital, in 75 of whom
Salmonella enterica
serotype Typhi grew. TUBEX performed best, achieving 94.7% sensitivity and 80.4% specificity. Typhidot, SD Bioline Typhoid, and Mega Salmonella were less specific and, in most cases, less sensitive.
Spoligotype Signatures in the
Mycobacterium tuberculosis
Complex
Authors: Streicher E. M. , Victor T. C. , van der Spuy G. , Sola C. , Rastogi N. , van Helden P. D. , Warren R. M. 
Published: December 2006

ABSTRACT

Evolution of the direct repeat region in
Mycobacterium tuberculosis
has created unique spoligotype signatures specifically associated with IS
6110-
defined strain families. Spoligotyping signatures may enable the analysis of the strain population structure in different settings and will enable the rapid identification of strain families that acquire drug resistance or escape protective immunity in drug and vaccine trials.
Helicobacter cinaedi
Cellulitis and Bacteremia in Immunocompetent Hosts after Orthopedic Surgery
Authors: Kitamura Toshio , Kawamura Yoshiaki , Ohkusu Kiyofumi , Masaki Takayuki , Iwashita Hirofumi , Sawa Tomohiro , Fujii Shigemoto , Okamoto Tatsuya , Akaike Takaaki 
Published: December 2006

ABSTRACT

At various times after orthopedic operations (more than a few weeks, with an average of 29.9 days), 11 patients had a sudden onset of high temperature (average 38.9°C) and local cellulitis at different sites on the operated sides. The wounds had completely healed, without complicated infections, when the cellulitis occurred. The clinical picture of cellulitis in all patients was atypical: diffuse salmon-pink skin color, local heat, swelling, spontaneous pain, and tenderness but no eruptions. No patient had any underlying immunocompromising conditions or had been given immunosuppressive agents. Gram-negative spiral bacteria were isolated from blood cultures and were identified as
Helicobacter cinaedi
on the basis of 16S rRNA gene sequencing and DNA-DNA hybridization using standard strains. By means of phylogenetic analysis, we divided these clinical isolates into two clones. The
H. cinaedi
strain isolated via fecal cultures from two patients without intestinal symptoms was the same clone as the blood isolate. All isolates were quite susceptible to various antibiotics, and clinical and inflammatory symptoms of bacteremia and cellulitis improved after treatment with penicillins and cephalosporins. A relatively high incidence of recurrence of the same disease was observed, however. Almost all patients responded immunologically to the infection, as evidenced by the production of serum antibody against
H. cinaedi
. We thus suggest that
H. cinaedi
should not be regarded as simply an opportunistic pathogen but that it may be a pathogen in immunocompetent hosts and may cause infections together with bacteremia and cellulitis.