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9 results on '"Sandu, Pamela"'

1. The Impact of Ferric Derisomaltose on Cardiovascular and Noncardiovascular Events in Patients With Anemia, Iron Deficiency, and Heart Failure With Reduced Ejection Fraction

Author

Kalra, Paul, Cowan, Elena, Howe, Serena, Turner, Charlotte, Austin, Rosalynn, Lane, Rebeca, Rogers, Paula, Foley, Paul, Chandrasekaran, Badri, Fraile, Eva, Kyeremeh, Lynsey, Ahmed, Fozia, Petrie, Mark, McGregor, Lorraine, Osmanska, Joanna, Graham, Fraser, Lang, Ninian, Meyer, Barbara, Ahmad, Faheem, Squire, Iain, Fisher, Jude, Kalra, Philip, Summersgill, Christina, Adeniji, Katarzyna, Chinnadurai, Rajkumar, Ludman, Andrew, Massimo, Lisa, Hardman, Clare, Sykes, Daisy, Cowburn, Peter, Frank, Sarah, Smith, Simon, Japp, Alan, Anwar, Mohamed, Whittington, Beth, Seed, Alison, Ray, Robin, Sookhoo, Vennessa, Al-Mohammad, Abdallah, Middle, Janet, Housley, Kay, Clark, Andrew, Bulemfu, Jeanne, Critoph, Christopher, Chong, Victor, Wood, Stephen, Szwejkowski, Benjamin, Lang, Chim, Duff, Jackie, MacDonald, Susan, Schiff, Rebekah, Donnelly, Patrick, Nageh, Thuraia, Kunhunny, Swapna, Gardner, Roy, McAdam, Marion, McPherson, Elizabeth, Banerjee, Prithwish, Sear, Eleanor, Edwards, Nigel, Glover, Jason, Pellicori, Pierpaolo, Murphy, Clare, Cooke, Justin, Spencer, Charles, Francis, Mark, Matthews, Iain, McKie, Hayley, Marshall, Andrew, Large, Janet, Stratford, Jenny, Clifford, Piers, Tavares, Sara, Boos, Christopher, Keeling, Philip, Hughes, Debbie, Wong, Aaron, Jones, Deborah, James, Alex, Williams, Rhys, Leslie, Stephen, Finlayson, Jim, Hannah, Andrew, Campbell, Philip, Walsh, John, Quinn, Jane, Chapman, Callum, Piper, Susan, Gupta, Preeti, Sim, Victor, Knibbs, Lucy, Lyons, Kristopher, Dixon, Lana, Petrie, Colin, Wong, Yuk-ki, Labinjoh, Catherine, Duckett, Simon, Massey, Ian, Savage, Henry, Matias, Sofia, Ramirez, Jonaifah, Manisty, Charlotte, Hussain, Ifza, Sankaranarayanan, Rajiv, Davis, Gershan, McClure, Samuel, Baxter, John, Wicks, Eleanor, Sobolewska, Jolanta, Murphy, Jerry, Elzayat, Ahmed, Cooke, Alastair, Wright, Jay, Williams, Simon, Muthumala, Amal, Chaggar, Parminder, Ellis, Gethin, Welch, Mandie, Bulugahapitiya, Sudantha, Jackson, Thomas, Pakrashi, Tapesh, Bakhai, Ameet, Gamma, Reto, Ellery, Susan, Jenkins, Geraint, Nightingale, Angus, Thomson, Elizabeth, Ford, Ian, Robertson, Michele, Greenlaw, Nicola, Wetherall, Kirsty, Clarke, Ross, Graham, Christopher, Kean, Sharon, Stevenson, Alan, Wilson, Robbie, Boyle, Sarah, McHugh, John, Hall, Lisa, Woollard, Joanne, Brunton, Claire, Dinnett, Eleanor, Reid, Amanda, Nicholls, Jill, Cunnington, Anna, Douglas, Elizabeth, Fegen, Margaret, Jones, Marc, McGowan, Sheila, Ross, Barbara, Sandu, Pamela, Surtees, Pamela, Stuart, Debra, Cleland, John G.F., Ahmed, Fozia Z., Cowburn, Peter J., Critoph, Chris, Kalra, Philip A., Lane, Rebecca E., Petrie, Mark C., Robertson, Michelle, and Kalra, Paul R.

Published
2024
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2. Intravenous ferric derisomaltose in patients with heart failure and iron deficiency in the UK (IRONMAN): an investigator-initiated, prospective, randomised, open-label, blinded-endpoint trial

Author

Kalra, Paul R, Cleland, John GF, Petrie, Mark C, Thomson, Elizabeth A, Kalra, Philip A, Squire, Iain B, Ahmed, Fozia Z, Al-Mohammad, Abdallah, Cowburn, Peter J, Foley, Paul WX, Graham, Fraser J, Japp, Alan G, Lane, Rebecca E, Lang, Ninian N, Ludman, Andrew J, Macdougall, Iain C, Pellicori, Pierpaolo, Ray, Robin, Robertson, Michele, Seed, Alison, Ford, Ian, Boon, Nicholas, Amoils, Shannon, Chapman, Callum, Diness, Thomas G, McMurray, John, Mindham, Richard, Sandu, Pamela, Strom, Claes C, Travers, Maureen, Wilcox, Robert, Struthers, Allan, Mark, Patrick, Weir, Christopher, Cowan, Elena, Turner, Charlotte, Austin, Rosalynn, Rogers, Paula, Chandrasekaran, Badri, Fraile, Eva, Kyeremeh, Lynsey, McGregor, Lorraine, Osmanska, Joanna, Meyer, Barbara, Ahmad, Faheem, Fisher, Jude, Summersgill, Christina, Adeniji, Katarzyna, Chinnadurai, Rajkumar, Massimo, Lisa, Hardman, Clare, Sykes, Daisy, Frank, Sarah, Smith, Simon, Anwar, Mohamed, Whittington, Beth, Sookhoo, Vennessa, Lyons, Sinead, Middle, Janet, Housley, Kay, Clark, Andrew, Bulemfu, Jeanne, Critoph, Christopher, Chong, Victor, Wood, Stephen, Szwejkowski, Benjamin, Lang, Chim, Duff, Jackie, MacDonald, Susan, Schiff, Rebekah, Donnelly, Patrick, Nageh, Thuraia, Kunhunny, Swapna, Gardner, Roy, McAdam, Marion, McPherson, Elizabeth, Banerjee, Prithwish, Sear, Eleanor, Edwards, Nigel, Glover, Jason, Murphy, Clare, Cooke, Justin, Spencer, Charles, Francis, Mark, Matthews, Iain, McKie, Hayley, Marshall, Andrew, Large, Janet, Stratford, Jenny, Clifford, Piers, Boos, Christopher, Keeling, Philip, Hughes, Debbie, Wong, Aaron, Jones, Deborah, James, Alex, Williams, Rhys, Leslie, Stephen, Finlayson, Jim, Hannah, Andrew, Campbell, Philip, Walsh, John, Quinn, Jane, Piper, Susan, Patale, Sheetal, Gupta, Preeti, Sim, Victor, Knibbs, Lucy, Lyons, Kristopher, Dixon, Lana, Petrie, Colin, Wong, Yuk-ki, Labinjoh, Catherine, Duckett, Simon, Massey, Ian, Savage, Henry, Matias, Sofia, Ramirez, Jonaifah, Manisty, Charlotte, Hussain, Ifza, Sankaranarayanan, Rajiv, Davis, Gershan, McClure, Samuel, Baxter, John, Wicks, Eleanor, Sobolewska, Jolanta, Murphy, Jerry, Elzayat, Ahmed, Cooke, Alastair, Wright, Jay, Williams, Simon, Muthumala, Amal, Chaggar, Parminder, Webber, Sue, Ellis, Gethin, Welch, Mandie, Bulugahapitiya, Sudantha, Jackson, Thomas, Pakrashi, Tapesh, Bakhai, Ameet, Krishnamurthy, Vinodh, Gamma, Reto, Ellery, Susan, Jenkins, Geraint, Thomas, Gladdys, Nightingale, Angus, Greenlaw, Nicola, Wetherall, Kirsty, Clarke, Ross, Graham, Christopher, Kean, Sharon, Stevenson, Alan, Wilson, Robbie, Boyle, Sarah, McHugh, John, Hall, Lisa, Woollard, Joanne, Brunton, Claire, Dinnett, Eleanor, Reid, Amanda, Howe, Serena, Nicholls, Jill, Cunnington, Anna, Douglas, Elizabeth, Fegen, Margaret, Jones, Marc, McGowan, Sheila, Ross, Barbara, Surtees, Pamela, Stuart, Debra, Cleland, John G F, and Foley, Paul W X

Published
2022
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3. The enterohaemorrhagic Escherichia coli effector EspW triggers actin remodelling in a Rac1 dependent manner

Author

Sandu, Pamela and Frankel, Gad

Subjects
570
Abstract

Enterohaemorrhagic Escherichia coli (EHEC) is a diarrheagenic pathogen that colonizes the gut mucosa by forming attaching-and-effacing lesions. EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack and manipulate host cell signalling pathways, which contribute to subversion of immune responses, colonization and disease. The role of many effectors during infection remains unclear. This study aimed to identify the function of the T3SS effector protein EspW. Although EspW is an EHEC effector, we found that it is present in the prototypes strains EPEC E11 and B171. Furthermore, screening a collection of clinical EPEC isolates revealed that espW is present in 52% of the tested stains, suggesting that EspW is an important virulence factor. We report that EspW modulates actin dynamics in a Rac1-dependant manner. Ectopic expression of EspW results in formation of unique membrane protrusions. Infection of Swiss cells with an EHEC espW deletion mutant induces cell shrinkage that could be overcomed by Rac1 activation via expression of the bacterial GEF, EspT. EspW contains a QLSI motif, similar to the QxSI sequence found in the catalytic loops of the effectors EspM and Map, which activate RhoA and Rac-1, respectively. We found that I237 within that motif is essential for the activity of EspW during ectopic expression and infection. Furthermore, using a yeast two hybrid screen we identified the motor protein Kif15 as a potential interacting partner of EspW. Kif15 and EspW co-localized in co-transfected cells, while ectopically expressed Kif15 localized to the actin pedestals following EHEC infection. The data suggest that Kif15 recruits EspW to the site of bacterial attachment, which in turn activates Rac1, resulting in modifications of the actin cytoskeleton that are essential to maintain cell shape during infection.

Published
2018
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4. The Enterohemorrhagic Escherichia coli effector EspW triggers actin remodeling in a Rac1-dependent manner

Author

Sandu, Pamela, Crepin, Valerie F, Drechsler, Hauke, McAinsh, Andrew D, Frankel, Gad, and Berger, Cedric N

Subjects
bacteria, biochemical phenomena, metabolism, and nutrition, QR
Abstract

Enterohemorrhagic Escherichia coli (EHEC) is a diarrheagenic pathogen that colonizes the gut mucosa and induces attaching-and-effacing lesions. EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack and manipulate host cell signaling pathways, which allow bacterial colonization and subversion of immune responses and disease progression. The aim of this study was to characterize the T3SS effector EspW. We found espW in the sequenced O157:H7 and non-O157 EHEC strains as well as in Shigella boydii. Furthermore, a truncated version of EspW, containing the first 206 residues, is present in EPEC strains belonging to serotype O55:H7. Screening a collection of clinical EPEC isolates revealed that espW is present in 52% of the tested strains. We report that EspW modulates actin dynamics in a Rac1-dependent manner. Ectopic expression of EspW results in formation of unique membrane protrusions. Infection of Swiss cells with an EHEC espW deletion mutant induces a cell shrinkage phenotype that could be rescued by Rac1 activation via expression of the bacterial guanine nucleotide exchange factor, EspT. Furthermore, using a yeast two-hybrid screen, we identified the motor protein Kif15 as a potential interacting partner of EspW. Kif15 and EspW colocalized in cotransfected cells, while ectopically expressed Kif15 localized to the actin pedestals following EHEC infection. The data suggest that Kif15 recruits EspW to the site of bacterial attachment, which in turn activates Rac1, resulting in modifications of the actin cytoskeleton that are essential to maintain cell shape during infection.

Published
2017

6. Campylobacter jejuni Outer Membrane Vesicles Play an Important Role in Bacterial Interactions with Human Intestinal Epithelial Cells

Author

Elmi, Abdi, primary, Watson, Eleanor, additional, Sandu, Pamela, additional, Gundogdu, Ozan, additional, Mills, Dominic C., additional, Inglis, Neil F., additional, Manson, Erin, additional, Imrie, Lisa, additional, Bajaj-Elliott, Mona, additional, Wren, Brendan W., additional, Smith, David G. E., additional, and Dorrell, Nick, additional

Published
2012
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7. Campylobacter jejuniOuter Membrane Vesicles Play an Important Role in Bacterial Interactions with Human Intestinal Epithelial Cells

Author

Elmi, Abdi, Watson, Eleanor, Sandu, Pamela, Gundogdu, Ozan, Mills, Dominic C., Inglis, Neil F., Manson, Erin, Imrie, Lisa, Bajaj-Elliott, Mona, Wren, Brendan W., Smith, David G. E., and Dorrell, Nick

Abstract

ABSTRACTCampylobacter jejuniis the most prevalent cause of food-borne gastroenteritis in the developed world; however, the molecular basis of pathogenesis is unclear. Secretion of virulence factors is a key mechanism by which enteric bacterial pathogens interact with host cells to enhance survival and/or damage the host. However, C. jejunilacks the virulence-associated secretion systems possessed by other enteric pathogens. Many bacterial pathogens utilize outer membrane vesicles (OMVs) for delivery of virulence factors into host cells. In the absence of prototypical virulence-associated secretion systems, OMVs could be an important alternative for the coordinated delivery of C. jejuniproteins into host cells. Proteomic analysis of C. jejuni11168H OMVs identified 151 proteins, including periplasmic and outer membrane-associated proteins, but also many determinants known to be important in survival and pathogenesis, including the cytolethal distending toxin (CDT). C. jejuniOMVs contained 16 N-linked glycoproteins, indicating a delivery mechanism by which these periplasm-located yet immunogenic glycoproteins can interact with host cells. C. jejuniOMVs possess cytotoxic activity and induce a host immune response from T84 intestinal epithelial cells (IECs), which was not reduced by OMV pretreatment with proteinase K or polymyxin B prior to coincubation with IECs. Pretreatment of IECs with methyl-beta-cyclodextrin partially blocks OMV-induced host immune responses, indicating a role for lipid rafts in host cell plasma membranes during interactions with C. jejuniOMVs. OMVs isolated from a C. jejuni11168H cdtAmutant induced interleukin-8 (IL-8) to the same extent as did wild-type OMVs, suggesting OMV induction of IL-8 is independent of CDT.

Published
2012
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8. The Enterohemorrhagic Escherichia coliEffector EspW Triggers Actin Remodeling in a Rac1-Dependent Manner

Author

Sandu, Pamela, Crepin, Valerie F., Drechsler, Hauke, McAinsh, Andrew D., Frankel, Gad, and Berger, Cedric N.

Abstract

ABSTRACTEnterohemorrhagic Escherichia coli(EHEC) is a diarrheagenic pathogen that colonizes the gut mucosa and induces attaching-and-effacing lesions. EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack and manipulate host cell signaling pathways, which allow bacterial colonization and subversion of immune responses and disease progression. The aim of this study was to characterize the T3SS effector EspW. We found espWin the sequenced O157:H7 and non-O157 EHEC strains as well as in Shigella boydii. Furthermore, a truncated version of EspW, containing the first 206 residues, is present in EPEC strains belonging to serotype O55:H7. Screening a collection of clinical EPEC isolates revealed that espWis present in 52% of the tested strains. We report that EspW modulates actin dynamics in a Rac1-dependent manner. Ectopic expression of EspW results in formation of unique membrane protrusions. Infection of Swiss cells with an EHEC espWdeletion mutant induces a cell shrinkage phenotype that could be rescued by Rac1 activation via expression of the bacterial guanine nucleotide exchange factor, EspT. Furthermore, using a yeast two-hybrid screen, we identified the motor protein Kif15 as a potential interacting partner of EspW. Kif15 and EspW colocalized in cotransfected cells, while ectopically expressed Kif15 localized to the actin pedestals following EHEC infection. The data suggest that Kif15 recruits EspW to the site of bacterial attachment, which in turn activates Rac1, resulting in modifications of the actin cytoskeleton that are essential to maintain cell shape during infection.

Published
2017
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9. The Enterohemorrhagic Escherichia coli Effector EspW Triggers Actin Remodeling in a Rac1-Dependent Manner.

Author

Sandu P, Crepin VF, Drechsler H, McAinsh AD, Frankel G, and Berger CN

Subjects
Animals, Cell Line, Humans, Kinesins metabolism, Mice, Protein Interaction Mapping, Two-Hybrid System Techniques, Actins metabolism, Enterohemorrhagic Escherichia coli pathogenicity, Escherichia coli Proteins metabolism, Host-Pathogen Interactions, rac1 GTP-Binding Protein metabolism
Abstract

Enterohemorrhagic Escherichia coli (EHEC) is a diarrheagenic pathogen that colonizes the gut mucosa and induces attaching-and-effacing lesions. EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack and manipulate host cell signaling pathways, which allow bacterial colonization and subversion of immune responses and disease progression. The aim of this study was to characterize the T3SS effector EspW. We found espW in the sequenced O157:H7 and non-O157 EHEC strains as well as in Shigella boydii Furthermore, a truncated version of EspW, containing the first 206 residues, is present in EPEC strains belonging to serotype O55:H7. Screening a collection of clinical EPEC isolates revealed that espW is present in 52% of the tested strains. We report that EspW modulates actin dynamics in a Rac1-dependent manner. Ectopic expression of EspW results in formation of unique membrane protrusions. Infection of Swiss cells with an EHEC espW deletion mutant induces a cell shrinkage phenotype that could be rescued by Rac1 activation via expression of the bacterial guanine nucleotide exchange factor, EspT. Furthermore, using a yeast two-hybrid screen, we identified the motor protein Kif15 as a potential interacting partner of EspW. Kif15 and EspW colocalized in cotransfected cells, while ectopically expressed Kif15 localized to the actin pedestals following EHEC infection. The data suggest that Kif15 recruits EspW to the site of bacterial attachment, which in turn activates Rac1, resulting in modifications of the actin cytoskeleton that are essential to maintain cell shape during infection., (Copyright © 2017 Sandu et al.)

Published
2017
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