Search

Your search keyword '"Leclercq, Sophie Y."' showing total 14 results
Start Over Author "Leclercq, Sophie Y."
14 results on '"Leclercq, Sophie Y."'

2. Synthesis of quinoline derivatives as potential cysteine protease inhibitors

Author

Andrade, Marina MS, primary, Martins, Luan C, additional, Marques, Gabriel VL, additional, Silva, Carla A, additional, Faria, Gilson, additional, Caldas, Sérgio, additional, dos Santos, Janete SC, additional, Leclercq, Sophie Y, additional, Maltarollo, Vinícius G, additional, Ferreira, Rafaela S, additional, and Oliveira, Renata B, additional

Published
2020
Full Text
View/download PDF

3. Effect of the Streptococcus agalactiae Virulence Regulator CovR on the Pathogenesis of Urinary Tract Infection

Author

Sullivan, Matthew J., Leclercq, Sophie Y., Ipe, Deepak S., Carey, Alison J., Smith, Joshua P., Voller, Nathan, Cripps, Allan W., and Ulett, Glen C.

Subjects
Cytotoxicity, Immunologic, Virulence Factors, Urinary Bladder, Gene Expression, Polymerase Chain Reaction, Bacterial Adhesion, Cell Line, Streptococcus agalactiae, Mice, Inbred C57BL, Mice, Bacterial Proteins, Urinary Tract Infections, Major Article, Animals, Cytokines, Humans, Female, Urothelium, Adhesins, Bacterial, Bacterial Capsules
Abstract

BACKGROUND. Streptococcus agalactiae can cause urinary tract infection (UTI). The role of the S. agalactiae global virulence regulator, CovR, in UTI pathogenesis is unknown. METHODS. We used murine and human bladder uroepithelial cell models of UTI and S. agalactiae mutants in covR and related factors, including β-hemolysin/cytolysin (β-h/c), surface-anchored adhesin HvgA, and capsule to study the role of CovR in UTI. RESULTS. We found that covR-deficient serotype III S. agalactiae 874391 was significantly attenuated for colonization in mice and adhesion to uroepithelial cells. Mice infected with covR-deficient S. agalactiae produced less proinflammatory cytokines than those infected with wild-type 874391. Acute cytotoxicity in uroepithelial cells triggered by covR-deficient but not wild-type 874391 was associated with significant caspase 3 activation. Mechanistically, covR mutation significantly altered the expression of several genes in S. agalactiae 874391 that encode key virulence factors, including β-h/c and HvgA, but not capsule. Subsequent mutational analyses revealed that HvgA and capsule, but not the β-h/c, exerted significant effects on colonization of the murine urinary tract in vivo. CONCLUSIONS. S. agalactiae CovR promotes bladder infection and inflammation, as well as adhesion to and viability of uroepithelial cells. The pathogenesis of S. agalactiae UTI is complex, multifactorial, and influenced by virulence effects of CovR, HvgA, and capsule.

Published
2016

9. Burkholderia pseudomallei Capsule Exacerbates Respiratory Melioidosis but Does Not Afford Protection against Antimicrobial Signaling or Bacterial Killing in Human Olfactory Ensheathing Cells

Author

Dando, Samantha J., primary, Ipe, Deepak S., additional, Batzloff, Michael, additional, Sullivan, Matthew J., additional, Crossman, David K., additional, Crowley, Michael, additional, Strong, Emily, additional, Kyan, Stephanie, additional, Leclercq, Sophie Y., additional, Ekberg, Jenny A. K., additional, St. John, James, additional, Beacham, Ifor R., additional, and Ulett, Glen C., additional

Published
2016
Full Text
View/download PDF

10. Lactococcus lactiscarrying the pValac DNA expression vector coding for IL-10 reduces inflammation in a murine model of experimental colitis

Author

Zurita-Turk, Meritxell, primary, del Carmen, Silvina, additional, Santos, Ana CG, additional, Pereira, Vanessa B, additional, Cara, Denise C, additional, Leclercq, Sophie Y, additional, de LeBlanc, Alejandra dM, additional, Azevedo, Vasco, additional, Chatel, Jean-Marc, additional, LeBlanc, Jean G, additional, and Miyoshi, Anderson, additional

Published
2014
Full Text
View/download PDF

13. Burkholderia pseudomalleiCapsule Exacerbates Respiratory Melioidosis but Does Not Afford Protection against Antimicrobial Signaling or Bacterial Killing in Human Olfactory Ensheathing Cells

Author

Dando, Samantha J., Ipe, Deepak S., Batzloff, Michael, Sullivan, Matthew J., Crossman, David K., Crowley, Michael, Strong, Emily, Kyan, Stephanie, Leclercq, Sophie Y., Ekberg, Jenny A. K., St. John, James, Beacham, Ifor R., and Ulett, Glen C.

Abstract

ABSTRACTMelioidosis, caused by the bacterium Burkholderia pseudomallei, is an often severe infection that regularly involves respiratory disease following inhalation exposure. Intranasal (i.n.) inoculation of mice represents an experimental approach used to study the contributions of bacterial capsular polysaccharide I (CPS I) to virulence during acute disease. We used aerosol delivery of B. pseudomalleito establish respiratory infection in mice and studied CPS I in the context of innate immune responses. CPS I improved B. pseudomalleisurvival in vivoand triggered multiple cytokine responses, neutrophil infiltration, and acute inflammatory histopathology in the spleen, liver, nasal-associated lymphoid tissue, and olfactory mucosa (OM). To further explore the role of the OM response to B. pseudomalleiinfection, we infected human olfactory ensheathing cells (OECs) in vitroand measured bacterial invasion and the cytokine responses induced following infection. Human OECs killed >90% of the B. pseudomalleiin a CPS I-independent manner and exhibited an antibacterial cytokine response comprising granulocyte colony-stimulating factor, tumor necrosis factor alpha, and several regulatory cytokines. In-depth genome-wide transcriptomic profiling of the OEC response by RNA-Seq revealed a network of signaling pathways activated in OECs following infection involving a novel group of 378 genes that encode biological pathways controlling cellular movement, inflammation, immunological disease, and molecular transport. This represents the first antimicrobial program to be described in human OECs and establishes the extensive transcriptional defense network accessible in these cells. Collectively, these findings show a role for CPS I in B. pseudomalleisurvival in vivofollowing inhalation infection and the antibacterial signaling network that exists in human OM and OECs.

Published
2016
Full Text
View/download PDF

14. Lactococcus lactis carrying the pValac DNA expression vector coding for IL-10 reduces inflammation in a murine model of experimental colitis.

Author

Zurita-Turk, Meritxell, del Carmen, Silvina, Santos, Ana CG, Pereira, Vanessa B., Cara, Denise C., Leclercq, Sophie Y., LeBlanc, Alejandra dM de, Azevedo, Vasco, Chatel, Jean-Marc, LeBlanc, Jean G, and Miyoshi, Anderson

Subjects
INFLAMMATORY bowel diseases, LACTOCOCCUS lactis, COLITIS, GASTROINTESTINAL system, MICE, FIBRONECTIN-binding proteins
Abstract

Background: Inflammatory bowel diseases (IBD) are intestinal disorders characterized by inflammation in the gastrointestinal tract. Interleukin-10 is one of the most important anti-inflammatory cytokines involved in the intestinal immune system and because of its role in downregulating inflammatory cascades, its potential for IBD therapy is under study. We previously presented the development of an invasive strain of Lactococcus lactis (L. lactis) producing Fibronectin Binding Protein A (FnBPA) which was capable of delivering, directly to host cells, a eukaryotic DNA expression vector coding for IL-10 of Mus musculus (pValac:il-10) and diminish inflammation in a trinitrobenzene sulfonic acid (TNBS)-induced mouse model of intestinal inflammation. As a new therapeutic strategy against IBD, the aim of this work was to evaluate the therapeutic effect of two L. lactis strains (the same invasive strain evaluated previously and the wild-type strain) carrying the therapeutic pValac:il-10 plasmid in the prevention of inflammation in a dextran sodium sulphate (DSS)-induced mouse model. Results: Results obtained showed that not only delivery of the pValac:il-10 plasmid by the invasive strain L. lactis MG1363 FnBPA+, but also by the wild-type strain L. lactis MG1363, was effective at diminishing intestinal inflammation (lower inflammation scores and higher IL-10 levels in the intestinal tissues, accompanied by decrease of IL-6) in the DSS-induced IBD mouse model. Conclusions: Administration of both L. lactis strains carrying the pValac:il-10 plasmid was effective at diminishing inflammation in this murine model of experimental colitis, showing their potential for therapeutic intervention of IBD. [ABSTRACT FROM AUTHOR]

Published
2014
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results