56 research outputs found

    Table_2_Wildlife Is a Potential Source of Human Infections of Enterocytozoon bieneusi and Giardia duodenalis in Southeastern China.XLSX

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    Wildlife is known to be a source of high-impact pathogens affecting people. However, the distribution, genetic diversity, and zoonotic potential of Cryptosporidium, Enterocytozoon bieneusi, and Giardia duodenalis in wildlife are poorly understood. Here, we conducted the first molecular epidemiological investigation of these three pathogens in wildlife in Zhejiang and Shanghai, China. Genomic DNAs were derived from 182 individual fecal samples from wildlife and then subjected to a nested polymerase chain reaction–based sequencing approach for detection and characterization. Altogether, 3 (1.6%), 21 (11.5%), and 48 (26.4%) specimens tested positive for Cryptosporidium species, E. bieneusi, and G. duodenalis, respectively. Sequence analyses revealed five known (BEB6, D, MJ13, SC02, and type IV) and two novel (designated SH_ch1 and SH_deer1) genotypes of E. bieneusi. Phylogenetically, novel E. bieneusi genotype SH_deer1 fell into group 6, and the other genotypes were assigned to group 1 with zoonotic potential. Three novel Cryptosporidium genotypes (Cryptosporidium avian genotype V-like and C. galli-like 1 and 2) were identified, C. galli-like 1 and 2 formed a clade that was distinct from Cryptosporidium species. The genetic distinctiveness of these two novel genotypes suggests that they represent a new species of Cryptosporidium. Zoonotic assemblage A (n = 36) and host-adapted assemblages C (n = 1) and E (n = 7) of G. duodenalis were characterized. The overall results suggest that wildlife act as host reservoirs carrying zoonotic E. bieneusi and G. duodenalis, potentially enabling transmission from wildlife to humans and other animals.</p

    Table_1_Wildlife Is a Potential Source of Human Infections of Enterocytozoon bieneusi and Giardia duodenalis in Southeastern China.DOCX

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    Wildlife is known to be a source of high-impact pathogens affecting people. However, the distribution, genetic diversity, and zoonotic potential of Cryptosporidium, Enterocytozoon bieneusi, and Giardia duodenalis in wildlife are poorly understood. Here, we conducted the first molecular epidemiological investigation of these three pathogens in wildlife in Zhejiang and Shanghai, China. Genomic DNAs were derived from 182 individual fecal samples from wildlife and then subjected to a nested polymerase chain reaction–based sequencing approach for detection and characterization. Altogether, 3 (1.6%), 21 (11.5%), and 48 (26.4%) specimens tested positive for Cryptosporidium species, E. bieneusi, and G. duodenalis, respectively. Sequence analyses revealed five known (BEB6, D, MJ13, SC02, and type IV) and two novel (designated SH_ch1 and SH_deer1) genotypes of E. bieneusi. Phylogenetically, novel E. bieneusi genotype SH_deer1 fell into group 6, and the other genotypes were assigned to group 1 with zoonotic potential. Three novel Cryptosporidium genotypes (Cryptosporidium avian genotype V-like and C. galli-like 1 and 2) were identified, C. galli-like 1 and 2 formed a clade that was distinct from Cryptosporidium species. The genetic distinctiveness of these two novel genotypes suggests that they represent a new species of Cryptosporidium. Zoonotic assemblage A (n = 36) and host-adapted assemblages C (n = 1) and E (n = 7) of G. duodenalis were characterized. The overall results suggest that wildlife act as host reservoirs carrying zoonotic E. bieneusi and G. duodenalis, potentially enabling transmission from wildlife to humans and other animals.</p

    AU4S: A novel synthetic peptide to measure the activity of ATG4 in living cells

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    <div><p>ATG4 plays a key role in autophagy induction, but the methods for monitoring ATG4 activity in living cells are limited. Here we designed a novel fluorescent peptide named AU4S for noninvasive detection of ATG4 activity in living cells, which consists of the cell-penetrating peptide (CPP), ATG4-recognized sequence “GTFG,” and the fluorophore FITC. Additionally, an ATG4-resistant peptide AG4R was used as a control. CPP can help AU4S or AG4R to penetrate cell membrane efficiently. AU4S but not AG4R can be recognized and cleaved by ATG4, leading to the change of fluorescence intensity. Therefore, the difference between AU4S- and AG4R-measured fluorescence values in the same sample, defined as “F-D value,” can reflect ATG4 activity. By detecting the F-D values, we found that ATG4 activity paralleled LC3B-II levels in rapamycin-treated cells, but neither paralleled LC3B-II levels in starved cells nor presented a correlation with LC3B-II accumulation in WBCs from healthy donors or leukemia patients. However, when DTT was added to the system, ATG4 activity not only paralleled LC3B-II levels in starved cells in the presence or absence of autophagy inhibitors, but also presented a positive correlation with LC3B-II accumulation in WBCs from leukemia patients (<i>R<sup>2</sup></i> = 0.5288). In conclusion, this study provides a convenient, rapid, and quantitative method to monitor ATG4 activity in living cells, which may be beneficial to basic and clinical research on autophagy.</p></div

    Extracellular Acidification Acts as a Key Modulator of Neutrophil Apoptosis and Functions

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    <div><p>In human pathological conditions, the acidification of local environment is a frequent feature, such as tumor and inflammation. As the pH of microenvironment alters, the functions of immune cells are about to change. It makes the extracellular acidification a key modulator of innate immunity. Here we detected the impact of extracellular acidification on neutrophil apoptosis and functions, including cell death, respiratory burst, migration and phagocytosis. As a result, we found that under the acid environment, neutrophil apoptosis delayed, respiratory burst inhibited, polarization augmented, chemotaxis differed, endocytosis enhanced and bacteria killing suppressed. These findings suggested that extracellular acidification acts as a key regulator of neutrophil apoptosis and functions.</p></div

    Galectin-8 Promotes Cytoskeletal Rearrangement in Trabecular Meshwork Cells through Activation of Rho Signaling

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    <div><h3>Purpose</h3><p>The trabecular meshwork (TM) cell-matrix interactions and factors that influence Rho signaling in TM cells are thought to play a pivotal role in the regulation of aqueous outflow. The current study was designed to evaluate the role of a carbohydrate-binding protein, galectin-8 (Gal8), in TM cell adhesion and Rho signaling.</p> <h3>Methods</h3><p>Normal human TM cells were assayed for Gal8 expression by immunohistochemistry and Western blot analysis. To assess the role of Gal8 in TM cell adhesion and Rho signaling, the cell adhesion and spreading assays were performed on Gal8-coated culture plates in the presence and the absence of anti-β<sub>1</sub> integrin antibody and Rho and Rho-kinase inhibitors. In addition, the effect of Gal8-mediated cell-matrix interactions on TM cell cytoskeleton arrangement and myosin light chain 2 (MLC2) phosphorylation was examined.</p> <h3>Principal Findings</h3><p>We demonstrate here that Gal8 is expressed in the TM and a function-blocking anti-β<sub>1</sub> integrin antibody inhibits the adhesion and spreading of TM cells to Gal8-coated wells. Cell spreading on Gal8 substratum was associated with the accumulation of phosphorylated myosin light chain and the formation of stress fibers that was inhibited by the Rho inhibitor, C3 transferase, as well as by the Rho-kinase inhibitor, Y27632.</p> <h3>Conclusions/Significance</h3><p>The above findings present a novel function for Gal8 in activating Rho signaling in TM cells. This function may allow Gal8 to participate in the regulation of aqueous outflow.</p> </div

    L'Écho : grand quotidien d'information du Centre Ouest

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    12 décembre 19371937/12/12 (A66)-1937/12/13.Appartient à l’ensemble documentaire : PoitouCh

    L'Écho : grand quotidien d'information du Centre Ouest

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    29 décembre 19141914/12/29 (A43).Appartient à l’ensemble documentaire : PoitouCh

    Extracellular acid enhance neutrophil endocytosis but suppress the bacteria killing ability.

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    <p>(A,B,C,D) Neutrophils endocytose FITC-Zymosan. 2×10<sup>6</sup> neutrophils were mixed with 1×10<sup>7</sup> opsonized FITC-Zymosan and co-incubated at 37°C for 30 min. Pictures were captured by a fluorescence microscope(600×). (A) Percentage of neutrophils happened to phagocytose. More than 100 cells were counted from random fields of each group. (B) Phagocytosis index was expressed as the number of the internalized particles per 100 neutrophils. (C) Binding index was expressed as the number of the binding particles per 100 neutrophils. (D) Fluorescence images of neutrophil phagocytosis. (E,F,G)Killing assay using neutrophils incubated with <i>E</i>.<i>Coli</i>.2×10<sup>6</sup> neutrophils were mixed with 1×10<sup>7</sup> opsonized <i>E</i>.<i>Coli</i> and co-incubated at 37°C for 30min. (E) Cells containing <i>E</i>.<i>Coli</i> were lysed, diluted and spread on the LB agar. CFUs of this group stand for the bacteria loading. Another two groups of neutrophils containing <i>E</i>.<i>Coli</i> were further incubated in the medium of pH 6.0 and pH 7.4 separately. After incubated for another 30 min, cells were lysed, diluted and spread on the LB agar. (F) The number of CFUs of each group were listed in the table. (G)</p><p></p><p></p><p>killing percentage<mo>=</mo></p><p><mo>(</mo></p><p><mn>1</mn><mo>-</mo></p><p></p><p>CFUs of pH 6.0/7.4</p><p>bacteria loading</p><p></p><p></p><mo>)</mo><p></p><mo>×</mo><mn>100</mn><mi>%</mi><p></p><p></p><p></p>. Data are from three independent experiments(A,B,C) or are representative of three experiments(D,E,F,G,H,I). (***,<i>p</i><0.001, **, <i>p</i><0.01, *,<i>p</i><0.05).<p></p
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