bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preliminary Human Study for Possible Alteration of Serum Immunoglobulin E Production in Perennial Allergic Rhinitis with Fermented Milk Prepared with Lactobacillus gasseri TMC0356
Authors: Morita Hirotsugu , He Fang , Kawase Manabu , Kubota Akira , Hiramatsu Masaru , Kurisaki Jun‐Ichi , Salminen Seppo 
Published: November 2013

AbstractThe fermented milk prepared with Lactobacillus gasseri TMC0356 was administered at 200 ml per day for 4 weeks to 15 subjects with high serum IgE levels and perennial allergic rhinitis. The serum total IgE concentration was significantly reduced after 28 days' exposure to the fermented milk (P<0.05) compared to that before the intervention. The serum IgE specific to Acari and those to Japanese cedar pollen also significantly declined (P<0.05). T helper 1 (Th1) cells in the composition of their peripheral blood mononuclear cells (PBMCs) significantly increased after 14 days (P<0.01) and after 28 days (P<0.05). These results suggest that the fermented milk prepared with L. gasseri TMC0356 may alter serum IgE concentration, at least partly by enhancement of Th1 immune responses of the subjects with high concentration of serum IgE. However, further studies are still necessary to know the underlying mechanisms by which the tested fermented milk could influence the host immunity.
A 4‐Aminofurazan Derivative—A189—Inhibits Assembly of Bacterial Cell Division Protein FtsZ In Vitro and In Vivo
Authors: Ito Hideaki , Ura Atsushi , Oyamada Yoshihiro , Tanitame Akihiko , Yoshida Hiroaki , Yamada Sakuo , Wachi Masaaki , Yamagishi Jun‐ichi 
Published: November 2013

AbstractOut of 95,000 commercially available chemical compounds screened by the anucleate cell blue assay, 138 selected hit compounds were further screened. As a result, A189, a 4‐aminofurazan derivative was found to inhibit FtsZ GTPase with an IC50 of 80 μg/ml and to exhibit antibacterial activity against Staphylococcus aureus and Escherichia coli. Light scattering demonstrated that A189 inhibited FtsZ assembly in vitro, and microscopic observation of A189‐treated E. coli indicated that A189 perturbed FtsZ ring formation and made bacterial cells filamentous. However, nucleoids staining with DAPI revealed that A189 did not affect DNA replication and chromosome segregation in bacterial filamentous cells. Furthermore, A189 made sulA‐deleted E. coli cells filamentous. Taken together, these findings suggest that A189 inhibits FtsZ GTPase activity, resulting in perturbation of FtsZ ring formation, which leads to bacterial cell death.
Detection of Enteroviruses and Mammalian Reoviruses in Korean Environmental Waters
Authors: Kim Hee Jung , Shin Young Oh , Kim Sang Hyun 
Published: November 2013

AbstractUsing the standard total culturable virus assay‐most probable number (TCVA‐MPN) method, we evaluated a total of 348 samples, including surface water, finished water, and tap water samples, collected from randomly selected water treatment plants in Korea from August 2001 through July 2005 according to the Information Collection Rule. All the TCVA‐positive samples were also subjected to integrated cell culture‐PCR (ICC‐PCR) methods for the detection of enteroviruses, hepatitis A virus, adenoviruses, and reoviruses. The most probable number of infectious units per 100 liters for the environmental water samples ranged from 0.5 to 47.3. Nine of the 13 TCVA‐positive samples (69.2%) were found by ICC‐PCR to be positive for human enteroviruses, which were confirmed to be coxsackievirus type B3, coxsackievirus type B4, coxsackievirus type B6, echovirus type 30, and vaccine strain poliovirus type 3 by direct sequencing. Eleven of the 13 TCVA‐positive samples (84.6%) were found by ICC‐PCR assay to be positive for reoviruses. The serotype of all the reoviruses was the same as reovirus type 1 by direct sequencing. Both enteroviruses and reoviruses were concurrently detected in seven TCVA‐positive samples (53.8%).
Human Herpesvirus‐6‐Specific Interleukin 10‐Producing CD4+ T Cells Suppress the CD4+ T‐Cell Response in Infected Individuals
Authors: Wang Fang , Yao Kun , Yin Quan‐Zhang , Zhou Feng , Ding Chuan‐Lin , Peng Guang‐Yong , Xu Jian , Chen Yun , Feng Dong‐Ju , Ma Chun‐Lin , Xu Wen‐Rong 
Published: November 2013

AbstractHuman herpesvirus‐6 (HHV‐6) infection normally persists for the lifetime of the host and may reactivate with immunosuppression. The mechanism behind HHV‐6 latent infection is still not fully understood. In this study, we observed that decreased proliferation of CD4+ T cells and PBMCs but not CD8+ T cells from HHV‐6‐infected individuals was stimulated with HHV‐6‐infected cell lysates. Moreover, HHV‐6‐stimulated CD4+ T cells from HHV‐6‐infected individuals have suppressive activity on naïve CD4+ T and CD8+ T cells from HHV‐6‐uninfected individuals. However, no increased proportion of CD4+ CD25+ Treg cells from HHV‐6‐infected individuals contributed to the suppressive activity of the HHV‐6‐stimulated CD4+ T cells from HHV‐6‐infected individuals. Transwell experiments, ELISA and anti‐IL‐10 antibody blocking experiment demonstrated that IL‐10 may be the suppressive cytokine required for suppressive activity of CD4+ T cells from HHV‐6‐infected individuals. Results of intracellular interleukin (IL)‐10 and IL‐4 further implicated the HHV‐6‐speciflc IL‐10‐producing CD4+ T cells in the suppressive activity of CD4+ T cells from HHV‐6‐infected individuals. Results of intracellular interferon (IFN)‐γ demonstrated a decreased frequency of HHV‐6‐speciflc IFN‐γ‐producing CD4+ T, but not CD8+ T cells in HHV‐6‐infected individuals, indicating that it was the CD4+ Th1 responses in HHV‐6‐infected individuals that were selectively impaired. Our findings indicated that HHV‐6‐specific IL‐10‐producing CD4+ T cells from HHV‐6‐infected individuals possess T regulatory type 1 cell activity: immunosuppression, high levels of IL‐10 production, with a few cells expressing IFN‐γ, but none expressing IL‐4. These cells may play an important role in latent HHV‐6 infection.
Human Milk Glycoproteins Inhibit the Adherence of Salmonella typhimurium to HeLa Cells
Authors: Bessler Heidi Christina , de Oliveira Inaiara Rosa , Giugliano Loreny Gimenes 
Published: November 2013

AbstractThe ability of human milk, as well as its protein fractions, to inhibit the adhesion and invasion of Salmonella typhimurium to HeLa cells was investigated. The results revealed that milk secretory immunoglobulin A (sIgA) inhibited neither the adherence nor the bacterial invasion; however, free secretory component and lactoferrin inhibited the bacterial adhesion and interacted with several bacterial proteins. Our data indicated that glycoproteins such as free secretory component and lactoferrin could act as protective compounds against infant enteric diseases, possibly binding to bacterial surface and blocking adhesion, the primordial step of S. typhimurium infection.
Autoimmune Regulator (AIRE) Gene Is Expressed in Human Activated CD4+ T‐Cells and Regulated by Mitogen‐Activated Protein Kinase Pathway
Authors: Nagafuchi Seiho , Katsuta Hitoshi , Koyanagi‐Katsuta Rimiko , Yamasaki Satoshi , Inoue Yasushi , Shimoda Kazuya , Ikeda Yukari , Shindo Mieko , Yoshida Eiko , Matsuo Tomohito , Ohno Yuju , Kogawa Kazuhiko , Anzai Keizo , Kurisaki Hironori , Kudoh Jun , Harada Mine , Shimizu Nobuyoshi 
Published: November 2013

AbstractThe autoimmune regulator (AIRE) gene is a gene responsible for autoimmune polyendocrinopathy‐candidiasis‐ectodermal dystrophy. Here we show that AIRE is expressed in human peripheral CD4‐positive T‐cells, and most highly in antigen‐ and interleukin 2‐stimulated T (IL‐2T) cells. Mitogen‐activated protein kinases (MAPKs), including MAPK kinase (MEK) 1/2 and p38 MAPK, were phosphorylated in IL‐2T cells and the expression of the AIRE gene was inhibited by a specific p38 MAPK inhibitor (SB203580), thereby indicating that AIRE gene expression is controlled by the MAPK pathway in IL‐2T cells. These data suggested the possible significance of the AIRE gene in the peripheral immune system.
In Vitro Infection of Immortalized Primary Hepatocytes by HCV Genotype 4a and Inhibition of Virus Replication by Cyclosporin
Authors: El‐Farrash Mohamed A. , Aly Hussein H. , Watashi Koichi , Hijikata Makoto , Egawa Hiroto , Shimotohno Kunitada 
Published: November 2013

AbstractHepatitis C virus (HCV) is a major cause of liver cirrhosis and hepatocellular carcinoma worldwide. We previously reported that cyclosporin A (CsA) inhibits HCV‐1b replication. However, its inhibition of JFH‐1 (HCV‐2a) was much less. Since HCV genotype clearly affects the in vitro and in vivo response to anti‐viral therapy, we wished to examine the effect of CsA and its non‐immunosuppressive derivative NIM811 on HCV genotype 4a replication. We first established an in vitro system supporting HCV‐4a infection and replication using immortalized human hepatocytes, HuS‐E7/DN24 (HuS) cells, and these cells were infected with sera obtained from Egyptian patients with chronic HCV‐4a infection. HuS cells supported more robust HCV‐4a replication than both HuH‐7.5 and PH5CH8 cells, and HCV‐4a infection and replication were completely inhibited by 3 μg/ml CsA and 0.5 μg/ml NIM811. Thus, HuS cells are a good model system supporting the infection and high‐level replication of HCV‐4a, and both CsA and NIM811 effectively inhibit HCV‐4a replication in this system.
The Relationship between Microbiota and Polyamine Concentration in the Human Intestine: A Pilot Study
Authors: Matsumoto Mitsuharu , Benno Yoshimi 
Published: November 2013

AbstractThe fecal microbiota of 10 hospitalized elderly subjects and 14 healthy adults were analyzed by terminal‐restriction fragment length polymorphism (T‐RFLP) analysis using HhaI, MspI, HaeIII, and AluI, as well as fecal polyamine (PA) concentration. The T‐RFLP profiles of the fecal microbiota of the subjects were roughly divided into 2 clusters—I (9 out of 11 were derived from hospitalized elderly subjects) and II (12 out of 13 were derived from healthy adults). The average concentration of putrescine in Cluster II was 5.8 times higher than that of putrescine in Cluster I (P=0.0015). Using a phylogenetic assignment database for T‐RFLP analysis of human colonic microbiota, the terminal‐restriction fragments (T‐RFs) characteristically detected in the case of subjects with high fecal PA concentration were predicted to be derived from bacterial species and phylotypes belonging to Clostridium subcluster XIVa, particularly including Clostridium xylanolyticum, Clostridium saccharolyticum, the uncultured human intestinal bacterium clone JW1H4 (a relative of Desulfotomaculum guttoideum), Roseburia intestinalis, the uncultured bacterium clone 41F10 (a relative of Eubacterium ramulus), Roseburia cecicola, Ruminococcus obeum and its relatives. From these results, we concluded that fecal microbiota may be linked with fecal PA concentration and that some bacterial species belonging to Clostridium subcluster XIVa may play a major role in the control of intestinal PA concentration in humans.
Comparison of Fecal Microbiota and Polyamine Concentration in Adult Patients with Intractable Atopic Dermatitis and Healthy Adults
Authors: Matsumoto Mitsuharu , Kakizoe Kenji , Benno Yoshimi 
Published: November 2013

AbstractFecal microbiota and polyamine concentration obtained from eleven intractable adult‐type atopic dermatitis (AD) patients and thirteen healthy adults were compared. Fecal microbiota were analyzed using terminal‐restriction fragment length polymorphism. The fecal microbiota of volunteers were divided into two clusters, A (n=16) and B (n=8), and the number of AD patients was found to be higher in Cluster B than Cluster A, suggesting that there are relationships between the obstinacy of intractable adult‐type AD and intestinal microbiota in Cluster B. Fecal spermidine concentration in Cluster B were lower than that in Cluster A significantly (P<0.05). Fecal putrescine concentration in Cluster B also tended to be lower than that in Cluster A. Terminal‐restriction fragment (T‐RF) of 122 bp generated by digestion with HhaI, which were predicted as unknown bacteria, were detected characteristically in Cluster A. In contrast, T‐RFs of 368/9 bp generated by digestion with HhaI, which were predicted as Enterobacteriaceae, were detected characteristically in Cluster B. These bacteria are closely associated with intestinal polyamine concentration. These findings raise the possibility that a low concentration of intestinal polyamines produced by intestinal microbiota is one of the important factors in the onset of intractable adult‐type AD.
Expression and Distribution of Very Late Antigen‐5 in Mouse Peritoneal Macrophages upon Ingestion of Fibronectin‐Bound Staphylococcus aureus
Authors: Shinji Hitomi , Kamada Minori , Seki Keiko , Tajima Akiko , Iwase Tadayuki , Masuda Shogo 
Published: November 2013

AbstractMany pathogens colonize host tissues by binding to the extracellular matrix via their cell surface adhesion molecules, which are called MSCRAMMs (microbial surface components recognizing adhesive matrix molecules). Staphylococcus aureus expresses several of these adhesion molecules, some of which bind to filbronectin. Of these adhesion molecules, filbronectin‐binding proteins play a role in the pathogenicity of S. aureus, although it is not yet clear whether they enhance its virulence. We have previously shown that filbronectin‐bound S. aureus is efficiently phagocytosed by thioglycolate‐induced mouse peritoneal macrophages. Bacterial ingestion is mediated by Very Late Antigen‐5 (VLA‐5; α5β1 integrin) and is accompanied by the formation of adhesion complexes. Here we show that the expression of VLA‐5 is restricted to thioglycolate‐induced inflammatory macrophages and is not found in the resident macrophages. When cells were in suspension, α5 integrin was not expressed on the surface of either resident or inflammatory macrophages, whereas in adherent cells, this integrin was distributed on the surface of inflammatory but not resident macrophages. A high level of this integrin was present in the cytoplasmic region only in inflammatory macrophages. In agreement with this, filbronectin‐mediated phagocytosis of S. aureus was observed only in the inflammatory macrophages. In inflammatory macrophages ingesting fibronectin‐bound S. aureus, α5 integrin was concentrated close to the phagocytosed bacteria. This change in distribution was not found in macrophages ingesting untreated bacteria. Together with our previous work, these results indicate that, upon ingestion of fibronectin‐bound S. aureus, VLA‐5 accumulates in the area of phagocytosis in inflammatory macrophages, where it forms adhesion complexes.
Effect of Interleukin‐10 on the Paracoccidioides brasiliensis Killing by Gamma‐Interferon Activated Human Neutrophils
Authors: Costa Diego Luís , Dias‐Melicio Luciane Alarcão , Acorci Michele Janegitz , Bordon Ana Paula , Tavian Elisandra Garcia , Peraçoli Maria Terezinha Serrão , de Campos Soares Angela Maria Victoriano 
Published: November 2013

AbstractParacoccidioidomycosis, a deep mycosis endemic in Latin America, is a chronic granulomatous disease caused by the fungus Paracoccidioides brasiliensis. Phagocytic cells play a critical role against this fungus, and several studies have shown the effects of activator and suppressive cytokines on macrophage and monocyte functions. However, studies on polymorphonuclear neutrophils (PMNs), that are the first cells recruited to the infection sites, are scarcer. Thus, the objective of this paper was to assess whether interleukin‐10 (IL‐10), a potent anti‐inflammatory cytokine, is able to block the activity of IFN‐γ‐activated human PMNs upon P. brasiliensis intracellular killing, in vitro. The results showed that IFN‐γ‐activated PMNs have an effective fungicidal activity against the fungus. This activity was associated with the release of high levels of H2O2, the metabolite involved in phagocytic cells antifungal activities. However, the concomitant incubation of these cells with IFN‐γ and IL‐10 significantly blocked IFN‐γ activation. As a consequence, PMNs killing activity and H2O2 release were inhibited. Together, our results show the importance of PMNs exposure to activator or suppressor cytokines in the early stages of paracoccidioidomycosis infection.
Beneficial Effect of GB Virus C Co‐Infection in Human Immunodeficiency Virus Type 1‐Infected Individuals
Authors: Hattori Junko , Okumura Naoya , Yamazaki Yumiko , Uchiyama Masataka , Hamaguchi Motohiro , Nishiyama Yukihiro , Kaneda Tsuguhiro 
Published: November 2013

AbstractSeveral reports have documented a better prognosis for HIV‐1‐infected patients co‐infected with GBV‐C, while other reports have contradicted such findings with the result that this issue remains controversial. We attempted to clarify the complicated status of the effect of GBV‐C co‐infection on HIV‐1‐infected patients. GBV‐C RNA was detected in 37 samples in 182 HIV‐1‐infected patients (20.3%) using RT/nested PCR. Of these, 3 were determined to be GBV‐C genotype 1, 12 were genotype 2, and the remaining 22 were genotype 3. The GBV‐C viral load quantified by real‐time PCR ranged from 7.8 × 103 to 3.3 × 106 copies/ml. Weakly negative correlation was observed between GBV‐C viral load and HIV‐1 viral load in 19 HAART‐naïve patients, indicating that a higher GBV‐C viral load is associated with a greater suppression of HIV‐1 replication. A previously published in vitro study suggested that GBV‐C infection would induce up‐regulation of RANTES, leading to suppression of HIV‐1 replication. However, in our present study, the blood RANTES level was significantly lower in the GBV‐C co‐infected group than in the uninfected group (190–9,959 vs. 264–31,038 pg/ml, P=0.004). Our results suggested that a suppression of HIV‐1 replication by GBV‐C co‐infection is not mediated by up‐regulated RANTES, and thus call for another as yet unknown factor.
A Correlation between Phagocytosis and Apoptosis in THP‐1 Cells Infected with Prevalent Strains of Mycobacterium tuberculosis
Authors: Rajavelu Priya , Das Sulochana D. 
Published: November 2013

AbstractThe innate ability of infected macrophages to undergo programmed cell death (apoptosis) and curtail the infection is crucial for the host defense. Although phagocytosis and intracellular killing mechanisms leading to apoptosis in macrophages are highly effective in eliminating the infecting tuberculous bacilli, some Mycobacterium tuberculosis (Mtb) strains have evolved strategies to inhibit this microbicidal function and make use of macrophage for its successful and prolonged survival. Two clinical strains of Mtb (S7 and S10) found to be prevalent and primitive, based on molecular epidemiological studies, were used to study the magnitude in induction of apoptosis in THP‐1 cells at various time points of infection and to correlate it with phagocytosis. The percentage of phagocytosis did not show any strain‐specific association with differentiated THP‐1 cells. But in the phagocytic index, the clinical strains showed a low dose of infection in the 1–10 bacilli category thereby exerting less burden on the cells. The induction of apoptosis was strain dependent The THP‐1 cells infected with H37Ra and S10 showed an increase in apoptosis at all time points while the S7 strain induced minimum apoptosis. A negative correlation between apoptosis and phagocytic index was observed in the 1–10 category and a positive correlation in the >20 category of the phagocytic index. This novel observation indicates that the magnitude of THP‐1 cell apoptosis is a function of the number of internalized mycobacteria. These results indicated a differential mode of infection by clinical strains and their adaptation to different survival strategies that may lead to immune suppression and pathogenesis of the disease.
A New Screening Method to Identify Inhibitors of the Lol (Localization of lipoproteins) System, a Novel Antibacterial Target
Authors: Ito Hideaki , Ura Atsushi , Oyamada Yoshihiro , Yoshida Hiroaki , Yamagishi Jun‐ichi , Narita Shin‐ichiro , Matsuyama Shin‐ichi , Tokuda Hajime 
Published: November 2013

AbstractAs the Lol system, which is involved in localization of lipoproteins, is essential for Escherichia coli growth and widely conserved among gram‐negative bacteria, it is considered to be a promising target for the development of anti‐gram‐negative bacterial agents. However, no high‐throughput screening method has so far been developed to screen for Lol system inhibitors. By combining three assay systems (anucleate cell blue assay, Lpp assay, and LolA‐dependent release inhibition assay) and a drug susceptibility test, we have successfully developed a new screening method for identification of compounds that inhibit the Lol system. Using this new screening method, we screened 23,600 in‐house chemical compounds and found 2 Lol system inhibitors. We therefore conclude that our new screening method can efficiently identify new antibacterial agents that target the Lol system.
DDX1 Promotes Proliferation of the JC Virus through Transactivation of Its Promoter
Authors: Sunden Yuji , Semba Shingo , Suzuki Tadaki , Okada Yuki , Orba Yasuko , Nagashima Kazuo , Umemura Takashi , Sawa Hirofumi 
Published: November 2013

AbstractRecently, we demonstrated that the DEAD box protein 1 (DDX1), an RNA helicase, and the cleavage stimulation factor (CstF) form a complex that binds to the JC virus transcriptional control region (JCV‐TCR). Here, we examined the function of DDX1, which is expressed at much higher levels in the JCV‐susceptible cell line IMR‐32 than in non‐susceptible cell lines. DDX1 had no effect on the replication efficiency of JCV, but over expression of DDX1 significantly increased transactivation of the JCV promoter. Furthermore, DDX1 enhanced the expression of JCV proteins in JCV infected cells, and knockdown of DDX1 using small interfering (si) RNA suppressed the expression of JCV proteins. Our results clearly demonstrate that DDX1 regulates proliferation of JCV in vitro through transcriptional activation.
Interferon‐Gamma Reverses the Evasion of Birc1e/Naip5 Gene Mediated Murine Macrophage Immunity by Legionella pneumophila Mutant Lacking Flagellin
Authors: Akamine Morikazu , Higa Futoshi , Haranaga Syusaku , Tateyama Masao , Mori Naoki , Heuner Klaus , Fujita Jiro 
Published: November 2013

AbstractLegionella pneumophila is the etiologic agent of Legionnaires' disease. This bacterium contains a single monopolar flagellum, of which the FlaA subunit is a major protein constituent The murine macrophage resistance against this bacterium is controlled by the Birc1e/Naip5 gene, which belongs to the NOD family. We evaluated the intracellular growth of the flaA mutant bacteria as well as another aflagellated fliA mutant, within bone marrow‐derived macrophages from mice with an intact (C57BL/6, BALB/c) or mutated (A/J) Birc1e/Naip5 gene. The flaA mutant L. pneumophila multiplied within C57BL/6 and BALB/c macrophages while the wild‐type strain did not Cell viability was not impaired until 3 days after infection when the flaA mutant bacteria replicated 102‐3‐fold in macrophages, implying that L. pneumophila inhibited host cell death during the early phase of intracellular replication. The addition of recombinant interferon‐gamma (IFN‐γ) to the infected macrophages restricted replication of the flaA mutant within macrophages; these treated cells also showed enhanced nitric oxide production, although inhibition of nitric oxide production did not affect the IFN‐γ induced inhibition of Legionella replication. These findings suggested that IFN‐γ activated macrophages to restrict the intracellular growth of the L. pneumophila flaA mutant by a NO independent pathway.