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4. Integrative omics identifies conserved and pathogen-specific responses of sepsis-causing bacteria

Author

Mu, Andre, Klare, William P., Baines, Sarah L., Ignatius Pang, C. N., Guérillot, Romain, Harbison-Price, Nichaela, Keller, Nadia, Wilksch, Jonathan, Nhu, Nguyen Thi Khanh, Phan, Minh-Duy, Keller, Bernhard, Nijagal, Brunda, Tull, Dedreia, Dayalan, Saravanan, Chua, Hwa Huat Charlie, Skoneczny, Dominik, Koval, Jason, Hachani, Abderrahman, Shah, Anup D., Neha, Nitika, Jadhav, Snehal, Partridge, Sally R., Cork, Amanda J., Peters, Kate, Bertolla, Olivia, Brouwer, Stephan, Hancock, Steven J., Álvarez-Fraga, Laura, De Oliveira, David M. P., Forde, Brian, Dale, Ashleigh, Mujchariyakul, Warasinee, Walsh, Calum J., Monk, Ian, Fitzgerald, Anna, Lum, Mabel, Correa-Ospina, Carolina, Roy Chowdhury, Piklu, Parton, Robert G., De Voss, James, Beckett, James, Monty, Francois, McKinnon, Jessica, Song, Xiaomin, Stephen, John R., Everest, Marie, Bellgard, Matt I., Tinning, Matthew, Leeming, Michael, Hocking, Dianna, Jebeli, Leila, Wang, Nancy, Ben Zakour, Nouri, Yasar, Serhat A., Vecchiarelli, Stefano, Russell, Tonia, Zaw, Thiri, Chen, Tyrone, Teng, Don, Kassir, Zena, Lithgow, Trevor, Jenney, Adam, Cole, Jason N., Nizet, Victor, Sorrell, Tania C., Peleg, Anton Y., Paterson, David L., Beatson, Scott A., Wu, Jemma, Molloy, Mark P., Syme, Anna E., Goode, Robert J. A., Hunter, Adam A., Bowland, Grahame, West, Nicholas P., Wilkins, Marc R., Djordjevic, Steven P., Davies, Mark R., Seemann, Torsten, Howden, Benjamin P., Pascovici, Dana, Tyagi, Sonika, Schittenhelm, Ralf B., De Souza, David P., McConville, Malcolm J., Iredell, Jonathan R., Cordwell, Stuart J., Strugnell, Richard A., Stinear, Timothy P., Schembri, Mark A., and Walker, Mark J.

Published
2023
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9. Neutrophil Extracellular Traps: An Emerging Therapeutic Target to Improve Infectious Disease Outcomes.

Author

Meier, Angela, Sakoulas, George, Nizet, Victor, and Ulloa, Erlinda R

Subjects
COVID-19, PROTEOLYTIC enzymes, COMMUNICABLE diseases, NATURAL immunity, DENGUE, COAT proteins (Viruses)
Abstract

Neutrophils possess a diverse repertoire of pathogen clearance mechanisms, one of which is the formation of neutrophil extracellular traps (NETs). NETs are complexes of histone proteins and DNA coated with proteolytic enzymes that are released extracellularly to entrap pathogens and aid in their clearance, in a process known as NETosis. Intravascular NETosis may drive a massive inflammatory response that has been shown to contribute to morbidity and mortality in many infectious diseases, including malaria, dengue fever, influenza, bacterial sepsis, and severe acute respiratory syndrome coronavirus 2 infection. In this review we seek to (1) summarize the current understanding of NETs, (2) discuss infectious diseases in which NET formation contributes to morbidity and mortality, and (3) explore potential adjunctive therapeutics that may be considered for future study in treating severe infections driven by NET pathophysiology. This includes drugs specifically targeting NET inhibition and US Food and Drug Administration–approved drugs that may be repurposed as NET inhibitors. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Efficacy of Alum-Adjuvanted Peptide and Carbohydrate Conjugate Vaccine Candidates against Group A Streptococcus Pharyngeal Infection in a Non-Human Primate Model.

Author

Rivera-Hernandez, Tania, Carnathan, Diane G., Richter, Johanna, Marchant, Patrick, Cork, Amanda J., Elangovan, Gayathiri, Henningham, Anna, Cole, Jason N., Choudhury, Biswa, Moyle, Peter M., Toth, Istvan, Batzloff, Michael R., Good, Michael F., Agarwal, Paresh, Kapoor, Neeraj, Nizet, Victor, Silvestri, Guido, and Walker, Mark J.

Subjects
PEPTIDES, STREPTOCOCCAL diseases, ARGININE deiminase, CARBOHYDRATES, ANTIBODY titer
Abstract

Vaccine development against group A Streptococcus (GAS) has gained traction in the last decade, fuelled by recognition of the significant worldwide burden of the disease. Several vaccine candidates are currently being evaluated in preclinical and early clinical studies. Here, we investigate two conjugate vaccine candidates that have shown promise in mouse models of infection. Two antigens, the J8 peptide from the conserved C-terminal end of the M protein, and the group A carbohydrate lacking N-acetylglucosamine side chain (ΔGAC) were each conjugated to arginine deiminase (ADI), an anchorless surface protein from GAS. Both conjugate vaccine candidates combined with alum adjuvant were tested in a non-human primate (NHP) model of pharyngeal infection. High antibody titres were detected against J8 and ADI antigens, while high background antibody titres in NHP sera hindered accurate quantification of ΔGAC-specific antibodies. The severity of pharyngitis and tonsillitis signs, as well as the level of GAS colonisation, showed no significant differences in NHPs immunised with either conjugate vaccine candidate compared to NHPs in the negative control group. [ABSTRACT FROM AUTHOR]

Published
2024
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21. The lytic polysaccharide monooxygenase CbpD promotes Pseudomonas aeruginosa virulence in systemic infection

Author

Askarian, Fatemeh, Uchiyama, Satoshi, Masson, Helen, Sørensen, Henrik Vinther, Golten, Ole, Bunæs, Anne Cathrine, Mekasha, Sophanit, Røhr, Åsmund Kjendseth, Kommedal, Eirik, Ludviksen, Judith Anita, Arntzen, Magnus Ø., Schmidt, Benjamin, Zurich, Raymond H., van Sorge, Nina M., Eijsink, Vincent G. H., Krengel, Ute, Mollnes, Tom Eirik, Lewis, Nathan E., Nizet, Victor, and Vaaje-Kolstad, Gustav

Published
2021
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24. Global chemical effects of the microbiome include new bile-acid conjugations

Author

Quinn, Robert A., Melnik, Alexey V., Vrbanac, Alison, Fu, Ting, Patras, Kathryn A., Christy, Mitchell P., Bodai, Zsolt, Belda-Ferre, Pedro, Tripathi, Anupriya, Chung, Lawton K., Downes, Michael, Welch, Ryan D., Quinn, Melissa, Humphrey, Greg, Panitchpakdi, Morgan, Weldon, Kelly C., Aksenov, Alexander, da Silva, Ricardo, Avila-Pacheco, Julian, Clish, Clary, Bae, Sena, Mallick, Himel, Franzosa, Eric A., Lloyd-Price, Jason, Bussell, Robert, Thron, Taren, Nelson, Andrew T., Wang, Mingxun, Leszczynski, Eric, Vargas, Fernando, Gauglitz, Julia M., Meehan, Michael J., Gentry, Emily, Arthur, Timothy D., Komor, Alexis C., Poulsen, Orit, Boland, Brigid S., Chang, John T., Sandborn, William J., Lim, Meerana, Garg, Neha, Lumeng, Julie C., Xavier, Ramnik J., Kazmierczak, Barbara I., Jain, Ruchi, Egan, Marie, Rhee, Kyung E., Ferguson, David, Raffatellu, Manuela, Vlamakis, Hera, Haddad, Gabriel G., Siegel, Dionicio, Huttenhower, Curtis, Mazmanian, Sarkis K., Evans, Ronald M., Nizet, Victor, Knight, Rob, and Dorrestein, Pieter C.

Published
2020
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30. Determining Susceptibility and Potential Mediators of Resistance for the Novel Polymyxin Derivative, SPR206, in Acinetobacter baumannii.

Author

Abdul-Mutakabbir, Jacinda C., Opoku, Nana Sakyi, Tan, Karen K., Jorth, Peter, Nizet, Victor, Fletcher, Hansel M., Kaye, Keith S., and Rybak, Michael J.

Subjects
ACINETOBACTER baumannii, POLYMYXIN, ACINETOBACTER infections, BACTERIAL cell walls, GENOMICS, ACTINOBACILLUS actinomycetemcomitans, SEQUENCE analysis, COLISTIN
Abstract

With the increase in carbapenem-resistant A. baumannii (CRAB) infections, there has been a resurgence in the use of polymyxins, specifically colistin (COL). Since the reintroduction of COL-based regimens in treating CRAB infections, several COL-resistant A. baumannii isolates have been identified, with the mechanism of resistance heavily linked with the loss of the lipopolysaccharide (LPS) layer of the bacterial outer membrane through mutations in lpxACD genes or the pmrCAB operon. SPR206, a novel polymyxin derivative, has exhibited robust activity against multidrug-resistant (MDR) A. baumannii. However, there is a dearth of knowledge regarding its efficacy in comparison with other A. baumannii-active therapeutics and whether traditional polymyxin (COL) mediators of A. baumannii resistance also translate to reduced SPR206 activity. Here, we conducted susceptibility testing using broth microdilution on 30 A. baumannii isolates (17 COL-resistant and 27 CRAB), selected 14 COL-resistant isolates for genomic sequencing analysis, and performed time-kill analyses on four COL-resistant isolates. In susceptibility testing, SPR206 demonstrated a lower range of minimum inhibitory concentrations (MICs) compared with COL, with a four-fold difference observed in MIC50 values. Mutations in lpxACD and/or pmrA and pmrB genes were detected in each of the 14 COL-resistant isolates; however, SPR206 maintained MICs ≤ 2 mg/L for 9/14 (64%) of the isolates. Finally, SPR206-based combination regimens exhibited increased synergistic and bactericidal activity compared with COL-based combination regimens irrespective of the multiple resistance genes detected. The results of this study highlight the potential utility of SPR206 in the treatment of COL-resistant A. baumannii infections. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Exploring Roles of the Polysaccharide Capsule in Pathogenesis of Hypervirulent Acinetobacter baumannii Clinical Isolate Lac-4.

Author

Bjånes, Elisabet, Koh, Truman, Qayum, Tariq, Zurich, Raymond, McCabe, Sinead, Hampel, Kegan, Cartwright, Lisa, and Nizet, Victor

Subjects
POLYSACCHARIDES, ACINETOBACTER baumannii, VENTILATOR-associated pneumonia, NOSOCOMIAL infections, DRUG development, ACTINOBACILLUS actinomycetemcomitans
Abstract

The frequently multidrug-resistant bacterial pathogen Acinetobacter baumannii is a leading cause of nosocomial infections, including ventilator-associated pneumonia, such that the World Health Organization and US Centers for Disease Control and Prevention have declared it a top priority candidate for novel drug development. Nearly all clinical A. baumannii strains express a thick surface polysaccharide capsule that protects against desiccation, host defenses, and disinfectants. In this study, we investigated the contribution of the polysaccharide capsule to virulence caused by the A. baumannii clinical isolate Ab Lac-4, which is rare in its ability to cause pneumonia and disseminated sepsis in healthy mice. We assessed the role of the capsule in wildtype Lac-4 (WT) by generating a premature stop codon in wza, which codes for the polysaccharide export protein. The wza# mutant was hypersensitive to killing by complement, whole blood, and healthy human neutrophils compared to WT and a revertant mutant (wza-Rev). Furthermore, the wza# mutant was highly attenuated in murine sepsis and unable to disseminate from the lungs during pneumonia. This study reinforces the capsule as a key contributor to Ab Lac-4 hypervirulence. [ABSTRACT FROM AUTHOR]

Published
2024
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35. Role of hypoxia inducible factor-1 in keratinocyte inflammatory response and neutrophil recruitment

Author

Leire, Emma, Olson, Josh, Isaacs, Hart, Nizet, Victor, and Hollands, Andrew

Abstract

Abstract Background Hypoxia inducible factor-1 (HIF-1) is a major regulator of the cellular adaption to low oxygen stress and the innate immune function of myeloid cells. Treatment with the novel HIF-1 stabilizing drug AKB-4924 has been shown to enhance the bactericidal activity of keratinocytes as well as phagocytic cells. In this study, we sought to investigate the effect of pharmacological boosting of HIF-1 with AKB-4924 in keratinocytes and their contribution to the innate immune response. Findings Treatment with the novel HIF-1 stabilizing drug AKB-4924 can increase keratinocyte production of pro-inflammatory cytokines in vitro and enhance neutrophil recruitment in vivo. Conclusions HIF plays an important role in cytokine production by keratinocytes and in neutrophil recruitment to the skin. The HIF-boosting drug AKB-4924 has the potential to enhance the immune response even in the complex environment of bacterial skin infections.

Published
2013

36. To NET or not to NET:current opinions and state of the science regarding the formation of neutrophil extracellular traps

Author

Boeltz, Sebastian, Amini, Poorya, Anders, Hans-Joachim, Andrade, Felipe, Bilyy, Rostyslav, Chatfield, Simon, Cichon, Iwona, Clancy, Danielle M., Desai, Jyaysi, Dumych, Tetiana, Dwivedi, Nishant, Gordon, Rachael Ann, Hahn, Jonas, Hidalgo, Andrés, Hoffmann, Markus H., Kaplan, Mariana J., Knight, Jason S., Kolaczkowska, Elzbieta, Kubes, Paul, Leppkes, Moritz, Manfredi, Angelo A., Martin, Seamus J., Maueröder, Christian, Maugeri, Norma, Mitroulis, Ioannis, Munoz, Luis E., Nakazawa, Daigo, Neeli, Indira, Nizet, Victor, Pieterse, Elmar, Radic, Marko Z, Reinwald, Christiane, Ritis, Konstantinos, Rovere-Querini, Patrizia, Santocki, Michal, Schauer, Christine, Schett, Georg, Shlomchik, Mark Jay, Simon, Hans-Uwe, Skendros, Panagiotis, Stojkov, Darko, Vandenabeele, Peter, Berghe, Tom Vanden, van der Vlag, Johan, Vitkov, Ljubomir, von Köckritz-Blickwede, Maren, Yousefi, Shida, Zarbock, Alexander, and Herrmann, Martin

Published
2019
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37. Prophage exotoxins enhance colonization fitness in epidemic scarlet fever-causing Streptococcus pyogenes

Author

Brouwer, Stephan, Barnett, Timothy C., Ly, Diane, Kasper, Katherine J., De Oliveira, David M. P., Rivera-Hernandez, Tania, Cork, Amanda J., McIntyre, Liam, Jespersen, Magnus G., Richter, Johanna, Schulz, Benjamin L., Dougan, Gordon, Nizet, Victor, Yuen, Kwok-Yung, You, Yuanhai, McCormick, John K., Sanderson-Smith, Martina L., Davies, Mark R., and Walker, Mark J.

Published
2020
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39. Study of the IgG endoglycosidase EndoS in group A streptococcal phagocyte resistance and virulence

Author

Sjögren, Jonathan, Okumura, Cheryl YM, Collin, Mattias, Nizet, Victor, and Hollands, Andrew

Abstract

Abstract Background The secreted enzyme EndoS, an endoglycosidase from Streptococcus pyogenes, hydrolyzes the N-linked glycan of the constant region of immunoglobulin G (IgG) heavy chain and renders the antibody unable to interact with Fc receptors and elicit effector functions. In this study we couple targeted allelic replacement mutagenesis and heterologous expression to elucidate the contribution of EndoS to group A Streptococcus (GAS) phagocyte resistance and pathogenicity in vitro and in vivo. Results Knocking out the EndoS gene in GAS M1T1 background revealed no significant differences in bacterial survival in immune cell killing assays or in a systemic mouse model of infection. However, exogenous addition and heterologous expression of EndoS was found to increase GAS resistance to killing by neutrophils and monocytes in vitro. Additionally, heterologous expression of EndoS in M49 GAS increased mouse virulence in vivo. Conclusions We conclude that in a highly virulent M1T1 background, EndoS has no significant impact on GAS phagocyte resistance and pathogenicity. However, local accumulation or high levels of expression of EndoS in certain GAS strains may contribute to virulence.

Published
2011

40. M1T1 group A streptococcal pili promote epithelial colonization but diminish systemic virulence through neutrophil extracellular entrapment

Author

Crotty Alexander, Laura E., Maisey, Heather C., Timmer, Anjuli M., Rooijakkers, Suzan H., Gallo, Richard L., Köckritz-Blickwede, Maren, and Nizet, Victor

Subjects
Biomedicine, Internal Medicine, Human Genetics, Molecular Medicine, Group A Streptococcus, Pilus, Virulence factor, IL-8, Neutrophil extracellular traps
Abstract

Group A Streptococcus is a leading human pathogen associated with a diverse array of mucosal and systemic infections. Cell wall anchored pili were recently described in several species of pathogenic streptococci, and in the case of GAS, these surface appendages were demonstrated to facilitate epithelial cell adherence. Here we use targeted mutagenesis to evaluate the contribution of pilus expression to virulence of the globally disseminated M1T1 GAS clone, the leading agent of both GAS pharyngitis and severe invasive infections. We confirm that pilus expression promotes GAS adherence to pharyngeal cells, keratinocytes, and skin. However, in contrast to findings reported for group B streptococcal and pneumococcal pili, we observe that pilus expression reduces GAS virulence in murine models of necrotizing fasciitis, pneumonia and sepsis, while decreasing GAS survival in human blood. Further analysis indicated the systemic virulence attenuation associated with pilus expression was not related to differences in phagocytic uptake, complement deposition or cathelicidin antimicrobial peptide sensitivity. Rather, GAS pili were found to induce neutrophil IL-8 production, promote neutrophil transcytosis of endothelial cells, and increase neutrophil release of DNA-based extracellular traps, ultimately promoting GAS entrapment and killing within these structures.

Published
2010

41. Accentuate the (Gram) positive

Author

Nizet, Victor

Subjects
Biomedicine, Internal Medicine, Human Genetics, Molecular Medicine, Gram-positive bacteria, Streptococcus, Special issue
Published
2010

45. Innate immunity turned inside-out: antimicrobial defense by phagocyte extracellular traps

Author

Köckritz-Blickwede, Maren and Nizet, Victor

Subjects
Biomedicine, Internal Medicine, Human Genetics, Molecular Medicine, Neutrophil, Mast cell, Eosinophil, Extracellular trap, Innate immunity, Bacterial infection, Virulence factors, Antimicrobial peptides, DNA, Histones, Mitochondria
Abstract

The formation of extracellular traps (ETs) by phagocytic cells has been recognized as a novel and important mechanism of the host innate immune response against infections. ETs are formed by different host immune cells such as neutrophils, mast cells, and eosinophils after stimulation with mitogens, cytokines, or pathogens themselves, in a process dependent upon induction of a reactive-oxygen-species-mediated signaling cascade. ETs consist of nuclear or mitochondrial DNA as a backbone with embedded antimicrobial peptides, histones, and cell-specific proteases and thereby provide a matrix to entrap and kill microbes and to induce the contact system. This review summarizes the latest research on ETs and their role in innate immunity and host innate defense. Attention is also given to mechanisms by which certain leading bacterial pathogens have evolved to avoid entrapment and killing in these specialized structures.

Published
2009

46. Cell death during sepsis: integration of disintegration in the inflammatory response to overwhelming infection

Author

Pinheiro da Silva, Fabiano and Nizet, Victor

Subjects
Biomedicine, Virology, Biochemistry, general, Oncology, Cell Biology, Cancer Research, Sepsis, Apoptosis, Cell necrosis, Pyroptosis, Extracellular traps, Lymphocyte, Macrophage, Bacterial infection
Abstract

Sepsis is a major health problem and a leading cause of death worldwide. In recent years, a crescendo of attention has been directed to the mechanisms of cell death that develop during this disease, since these are viewed as important contributors to the proinflammatory and anti-inflammatory responses associated with poor outcome. Here we discuss mechanisms of cell death evident severe bacterial infection and sepsis including necrosis, apoptosis, pyroptosis, and extracellular trap-associated neutrophil death, with a particular emphasis on lymphocyte apoptosis and its contribution to the immunosuppressed phenotype of late sepsis. Individual bacterial pathogens express virulence factors that modulate cell death pathways and influence the sepsis phenotype. A greater knowledge of cell death pathways in sepsis informs the potential for future therapies designed to ameliorate immune dysfunction in this syndrome.

Published
2009

47. Genetic Characterization of Streptococcus pyogenes emm89 Strains Isolated in Japan From 2011 to 2019

Author

Hirose, Yujiro, Yamaguchi, Masaya, Takemoto, Norihiko, Miyoshi-Akiyama, Tohru, Sumitomo, Tomoko, Nakata, Masanobu, Ikebe, Tadayoshi, Hanada, Tomoki, Yamaguchi, Takahiro, Kawahara, Ryuji, Okuno, Rumi, Otsuka, Hitoshi, Matsumoto, Yuko, Terashima, Yuji, Kazawa, Yu, Nakanishi, Noriko, Uchida, Kaoru, Akiyama, Yumi, Iwabuchi, Kaori, Nakagawa, Chikara, Yamamoto, Kazunari, Nizet, Victor, and Kawabata, Shigetada

Published
2020
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