Vincenzo Torraca

@kcl.ac.uk

Lecturer in Infectious Disease, Department of Infectious Diseases
King's College London

Vincenzo Torraca


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https://researchid.co/vincenzo.torraca
I am a Lecturer in Infectious Disease at King's College London and a Fellow of the Higher Education Academy (FHEA). My research focuses on host-pathogen interactions, genomic epidemiology, and antimicrobial resistance for globally relevant bacterial pathogens. In my lab, we use the zebrafish model to recapitulate human infections with a variety of bacteria, including Shigella, E. coli, Salmonella, and Mycobacterium. We are also interested in cell biology and we explore infections as a tool to obtain a better understanding of cell functions in both physiological and pathological contexts. Over the last few years, my work focused on the persistent carriage of enteropathogens and on the development of innovative strategies to counteract Shigella infections.

EDUCATION

I was awarded a Postgraduate Certificate in Learning and Teaching (LSHTM), a PhD in Microbiology and Immunology (Leiden University), a MSc in Molecular and Cellular Biology (Salerno University) and a BSc in Molecular and Computational Biology (Salerno University).

I was previously a Senior Lecturer in Microbiology and Co-Course Leader for BSc (Hons) Medical Sciences at the University of Westminster, an Assistant Professor and Wellcome ISSF Fellow at the London School of Hygiene and Tropical Medicine, a Marie Curie Research Fellow at Imperial College London and a Marie Curie PhD Fellow at Leiden University.

RESEARCH, TEACHING, or OTHER INTERESTS

Infectious Diseases, Immunology and Microbiology, Animal Science and Zoology, Medicine
43

Scopus Publications

2129

Scholar Citations

25

Scholar h-index

31

Scholar i10-index

Scopus Publications

  • Genome-wide analysis exploring mechanisms used by Shigella sonnei to survive long-term nutrient starvation
    Xosé M. Matanza, P. Brian Leung, Vincenzo Torraca, Jayne Watson, Matthew J. Dorman, Nicholas R. Thomson, Abigail Clements
    Msystems, 2026
    Shigella is a major cause of severe diarrhea, with Shigella flexneri and Shigella sonnei accounting for over 90% of infections. Progressive economic growth worldwide correlates with the replacement of S. flexneri by S. sonnei as the dominant cause of shigellosis. The basis of the epidemiological shift remains unclear, but it highlights the urgent need for further studies on the increasingly prevalent, but less well-studied, S. sonnei . Here, we investigated whether S. sonnei is better equipped to survive nutrient starvation, a crucial condition for persistence both outside the host and within the colonic lumen. S. sonnei exhibited greater survival under long-term nutrient starvation (LTNS) than S. flexneri , rapidly activating survival mechanisms. We interrogated the genome of S. sonnei using transposon-directed insertion-site sequencing (TraDIS), revealing that metabolic pathways (ATP, nucleotide, and amino acid synthesis) and envelope homeostasis systems (e.g., Tol-Pal complex, Bam complex, peptidoglycan recycling, and RpoE stress response) are conditionally essential for LTNS. TraDIS findings were validated by non-competitive and competitive survival of wild-type and deletion mutant strains. We compared the homology of conditionally essential genes between S. sonnei and S. flexneri to identify genes potentially involved in differential LTNS survival between the species. However, S. sonnei strains in which a single gene was replaced with the S. flexneri allele showed wild-type survival phenotypes. This suggests that the divergent survival of these two species may be more complex than a monogenic difference. Together, these data define the molecular adaptations of starvation resistance in S. sonnei and provide insights into its epidemiological dominance in high-income countries. IMPORTANCE Understanding why Shigella sonnei has a higher prevalence than Shigella flexneri as a country undergoes economic growth is an important challenge in Shigella research. The investigation of their biological and genetic differences is key to tackling the impact of the disease. We discovered that S. sonnei resists nutrient deprivation better than S. flexneri , suggesting a better adaptation to an extracellular lifestyle and a greater preservation of metabolic capabilities. Using a genome-wide transposon sequencing approach, we uncovered the key pathways behind the survival of S. sonnei facing nutrient starvation, which include ATP, nucleotide, and amino acid synthesis as well as maintenance of cell envelope integrity. Comparative analysis between S. sonnei and S. flexneri did not identify an individual gene responsible for the differing survival and may reflect a multifactorial difference. Our data provide a genome-wide basis for understanding how S. sonnei is adapted to nutrient-deprived settings, which may be advantageous in the gut lumen and for environmental survival, potentially contributing to its dominance in high-income countries.
  • Population structure, antimicrobial resistance, and virulence factors of diabetic foot-associated Escherichia coli
    Victor Ajumobi, Zaid Tahir, Polly Hayes, Adele McCormick, Vincenzo Torraca
    Microbiology Spectrum, 2026
    Diabetic foot infections (DFIs) are a major complication of diabetes, often leading to lower limb amputations. Escherichia coli is a predominant Gram-negative pathogen in DFI, yet its genomic and pathogenic features remain poorly characterized. Here, we present a whole-genome sequence-based analysis of diabetic foot-associated E. coli (DFEC) isolates from diverse geographical locations. Phylogenetic reconstruction revealed substantial diversity, with strains spanning 7 phylogroups and 28 sequence types. Capsule biosynthesis loci linked to invasive infections, such as K1, K2ab, and K5, were also detected. The DFEC pangenome comprised 18,263 gene clusters, indicating high genomic plasticity. The plasmid repertoire was also varied and contributed to the genomic diversity of the strains. Approximately 78% of isolates were multidrug-resistant or extensively drug-resistant, with resistance to last-resort antibiotics such as colistin and carbapenems also observed. High frequencies of virulence factors involved in host cell adherence, iron metabolism, serum survival, as well as toxins and type 3 secretion system genes were also detected. In contrast, metabolic modeling showed conserved biochemical profiles. Clustering based on accessory metabolic functions did not mirror phylogeny, suggesting metabolic convergence among distinct lineages. Collectively, these findings reveal that DFEC are versatile pathogens with a repertoire of antimicrobial resistance and virulence determinants. These traits make them functionally distinct from commensal E. coli strains and highlight the potential of DFEC to cause severe and invasive infections. IMPORTANCE This study presents the first multisite genomic characterization of diabetic foot-associated Escherichia coli (DFEC). Our findings reveal that DFEC strains are phylogenetically diverse and span multiple lineages. The high prevalence of multidrug-resistant and extensively drug-resistant genotypes underscores the underestimated antimicrobial resistance (AMR) threat posed by DFEC. We detect high frequencies of virulence factors commonly associated with extraintestinal pathogenic E. coli , which indicates that DFEC might have the potential to cause severe complications, such as sepsis. The large accessory genome and evidence of metabolic convergence across distinct lineages highlight the adaptive versatility of DFEC in the polymicrobial and inflammatory environment of chronic wounds. These insights advance our understanding of DFEC pathobiology and support the development of targeted diagnostics, AMR surveillance, and therapeutic strategies to improve clinical outcomes for diabetic patients.
  • A public resource of 15 genomically characterized representative strains of Shigella sonnei
    Sydney L. Miles, Jane Hawkey, Ben Vezina, Vincenzo Torraca, Claire Jenkins, François-Xavier Weill, Stephen Baker, Kate S. Baker, Serge Mostowy, Kathryn E. Holt
    Microbial Genomics, 2026
    Shigella sonnei is rapidly emerging as the dominant agent of shigellosis, an enteric disease responsible for a significant burden of morbidity and mortality worldwide. Whole-genome sequencing of S. sonnei isolated over the last three decades has revealed phylogenomic diversity within the population and the emergence of multiple lineages associated with distinct epidemiological patterns such as resistance to critical antimicrobials and/or transmission within different groups. However, most experimental work on S. sonnei biology and pathogenicity has focused on a single laboratory strain (53G), which is phylogenetically distant from currently circulating strains. Here, we introduce a set of phylogenetically diverse and epidemiologically relevant S. sonnei isolates made available through publicly accessible culture collections as a resource for laboratory science. We present their complete whole-genome sequences, including the pINV invasion plasmid (missing from a large proportion of public genome data due to loss during laboratory culture). Finally, the characterization and comparison of these complete genome sequences highlight evidence for ongoing adaptive evolution in S. sonnei , featuring the accumulation of insertion sequences, gene pseudogenization and structural variation.
  • Enhanced virulence and stress tolerance are signatures of epidemiologically successful Shigella sonnei
    Sydney L. Miles, Dilys Santillo, Hannah Painter, Kathryn Wright, Vincenzo Torraca, Ana T. López-Jiménez, Mollie Virgo, Xosé M. Matanza, Abigail Clements, Claire Jenkins, Stephen Baker, Kate S. Baker, David Cisneros, Andrea Puhar, Vanessa Sancho-Shimizu, Kathryn E. Holt, Serge Mostowy
    Nature Communications, 2025
    Shigellosis is a leading cause of diarrhoeal deaths, with Shigella sonnei increasingly implicated as a dominant agent. S. sonnei is divided into five monophyletic lineages, yet most infections are caused by a few clonal sub-lineages within Lineage 3 that are quite distinct from the widely used Lineage 2 laboratory strain 53G. Factors underlying the success of these globally dominant lineages remain unclear in part due to a lack of complete genome sequences and animal models. Here, we utilise a novel reference collection of representative Lineage 1, 2 and 3 isolates and find that epidemiologically successful S. sonnei harbour fewer genes encoding putative immunogenic components whilst key virulence-associated regions (including the type three secretion system and O-antigen) remain highly conserved. Using a zebrafish infection model, Lineage 3 isolates proved most virulent, driven by increased dissemination and a greater neutrophil response. These isolates also show increased resistance to complement-mediated killing alongside upregulated expression of group four capsule synthesis genes. Consistently, primary human neutrophil infections revealed an increased tolerance to phagosomal killing. Together, our findings link the epidemiological success of S. sonnei to heightened virulence and stress tolerance, and highlight zebrafish as a valuable platform to illuminate factors underlying establishment of epidemiological success.
  • DRAM1 promotes the stability of lysosomal VAMP8 to enhance autolysosome formation and facilitates the extravasation
    Rui Zhang, Xin Zhang, Hua Bai, Qiuyu Cheng, Xia Yao, Shi Li, Vincenzo Torraca, Chaojun Yan, Xueying Dong, Siyi Miao, Xueyuan Hu, Yeping Yu, Yueyan Wu, Hongfei Tan, Xin Chen, Shicheng Liu, Hao Lyu, Shuai Xiao, Dong Guo, Qi Zhang, Xing-Zhen Chen, Zhiyin Song, Cefan Zhou, Jingfeng Tang
    Nature Communications, 2025
    Autophagy classically functions to protect cells and organisms during stressful conditions by catabolizing intracellular components to maintain energy homeostasis. Lysosome-autophagosome fusion is a critical step in emptying degraded unwanted contents. However, the mechanism of autophagosome fusion with lysosomes is still not fully understood. Here, we report that DNA Damage-Regulated Autophagy Modulator 1 (DRAM1) interacts with Vesicle Associated Membrane Protein 8 (VAMP8) to mediate the fusion of autophagosomes with lysosomes. This DRAM1-VAMP8 interaction is enhanced upon stimulation of autophagy. However, DRAM1 preferentially mediates the fusion between autophagosomes and lysosomes by enhancing the assembly of the STX17-SNAP29-VAMP8 complex. Moreover, we reveal that DRAM1 specifically promotes the stability of lysosomal VAMP8 via inhibiting VAMP8 degradation by CHIP mediating ubiquitination. We also identify that DRAM1 inhibits the ubiquitination of VAMP8 at Lys 68,72, and 75 via competitively binding with CHIP. Furthermore, we demonstrate that DRAM1 promotes the extravasation of Hepatocellular Carcinoma (HCC) cells, and this process relies on enhanced autophagosome degradation. Our study reveals a mechanism for regulating autolysosome formation by DRAM1-VAMP8 association and suggests a potential strategy to inhibit the extravasation of HCC.
  • VAMP8 stabilization by DRAM1 enables autophagosome-lysosome fusion and promotes metastatic extravasation
    Rui Zhang, Vincenzo Torraca, Chaojun Yan, Hao Lyu, Shuai Xiao, Dong Guo, Qi Zhang, Cefan Zhou, Jingfeng Tang
    Autophagy, 2025
    Autophagosome-lysosome fusion, essential for macroautophagy/autophagy completion, requires the STX17-SNAP29-VAMP8 SNARE complex. While VAMP8 is crucial, its regulatory mechanisms remain incompletely understood. Here, we identify DRAM1 (DNA damage regulated autophagy modulator 1) as a key interactor and stabilizer of VAMP8 on lysosomes. In this study, we demonstrated that DRAM1 directly binds VAMP8, and this interaction is enhanced during autophagy induction. Mechanistically, DRAM1 inhibits ubiquitin-mediated degradation of lysosomal VAMP8 by the E3 ligase STUB1/CHIP to enhance autolysosome formation. DRAM1 competitively binds VAMP8 within residues 66–100 aa, shielding lysines 68, 72, and 75 from STUB1-mediated ubiquitination. This stabilization promotes assembly of the STX17-SNAP29-VAMP8 complex, enhancing autophagosome-lysosome fusion. Functionally, DRAM1-mediated VAMP8 stabilization and autophagic flux promote the extravasation and metastasis of hepatocellular carcinoma (HCC) cells in vitro and in vivo (mouse and zebrafish models). Depletion of core autophagy genes (ATG5 or ATG7) abolishes DRAM1’s pro-metastatic effects. Our findings reveal a novel DRAM1-VAMP8 axis that regulates autophagic flux and identify DRAM1 as a potential therapeutic target for inhibiting autophagy-dependent HCC metastasis. Here, we summarize our findings and discuss their implications for our understanding of autophagy regulation.
  • ILKAP Promotes the Metastasis of Hepatocellular Carcinoma Cells by Inhibiting β-Catenin Degradation and Enhancing the WNT Signaling Pathway
    Rui Zhang, Jinglei Yuan, Shicheng Liu, Vincenzo Torraca, Zhiquan Liao, Yueyan Wu, Hongfei Tan, Xia Yao, Xueyang Hou, Hao Lyu, Shuai Xiao, Dong Guo, Declan William Ali, Marek Michalak, Xing‐Zhen Chen, Cefan Zhou, Jingfeng Tang
    Advanced Biology, 2024
    The incidence of Hepatocellular carcinoma (HCC) and HCC‐related deaths have remarkably increased over the recent decades. It has been reported that β‐catenin activation can be frequently observed in HCC cases. This study identified the integrin‐linked kinase‐associated phosphatase (ILKAP) as a novel β‐catenin‐interacting protein. ILKAP is localized both in the nucleus and cytoplasm and regulates the WNT pathway in different ways. First, it is demonstrated that ILKAP activates the WNT pathway in HCC cells by increasing the protein level of β‐catenin and other proteins associated with the WNT signaling, such as c‐Myc and CyclinD1. Next, it is shown that ILKAP promotes the metastasis of HCC both in vitro and in vivo in a zebrafish xenograft model. It is also found that ILKAP dephosphorylates the GSK3β and CK1, contributing to the reduced ubiquitination of β‐catenin. Furthermore, it is identified that ILKAP functions by mediating binding between TCF4 and β‐catenin to enhance expression of WNT target genes. Taken together, the study demonstrates a critical function of ILKAP in metastasis of HCC, since ILKAP is crucial for the activation of the WNT pathway via stabilization of β‐catenin and increased binding between TCF4 and β‐catenin.
  • RUNDC1 negatively mediates the fusion of autophagosomes with lysosomes via regulating SNARE complex assembly
    Rui Zhang, Vincenzo Torraca, Hao Lyu, Shuai Xiao, Dong Guo, Cefan Zhou, Jingfeng Tang
    Autophagy, 2024
    Macroautophagy/autophagy is an essential pro-survival mechanism activated in response to nutrient deficiency. The proper fusion between autophagosomes and lysosomes is a critical step for autophagic degradation. We recently reported that RUNDC1 (RUN domain containing 1) inhibits autolysosome formation via clasping the ATG14-STX17-SNAP29 complex to hinder VAMP8 binding. We showed that RUNDC1 colocalizes with LC3 and associates with mature autophagosomes in cell lines and the zebrafish model. We utilized liposome fusion and in vitro autophagosome-lysosome fusion assays to demonstrate that RUNDC1 inhibits autolysosome formation. Moreover, we found that RUNDC1 clasps the ATG14-STX17-SNAP29 complex via stimulating ATG14 homo-oligomerization to inhibit ATG14 dissociation, which in turn prevents VAMP8 from binding to STX17-SNAP29. Our results demonstrate that RUNDC1 is a negative regulator of autophagy that restricts autophagosome fusion with lysosomes and is crucial for zebrafish survival in nutrient-deficient conditions. Here, we summarize our findings and discuss their implications for our understanding of autophagy regulation.
  • Transcriptional profiling of zebrafish identifies host factors controlling susceptibility to Shigella flexneri
    Vincenzo Torraca, Richard J. White, Ian M. Sealy, Maria Mazon-Moya, Gina Duggan, Alexandra R. Willis, Elisabeth M. Busch-Nentwich, Serge Mostowy
    Dmm Disease Models and Mechanisms, 2024
    Shigella flexneri is a human-adapted pathovar of Escherichia coli that can invade the intestinal epithelium, causing inflammation and bacillary dysentery. Although an important human pathogen, the host response to S. flexneri has not been fully described. Zebrafish larvae represent a valuable model for studying human infections in vivo. Here, we use a Shigella-zebrafish infection model to generate mRNA expression profiles of host response to Shigella infection at the whole-animal level. Immune response-related processes dominate the signature of early Shigella infection (6 h post-infection). Consistent with its clearance from the host, the signature of late Shigella infection (24 h post-infection) is significantly changed, and only a small set of immune-related genes remain differentially expressed, including acod1 and gpr84. Using mutant lines generated by ENU, CRISPR mutagenesis and F0 crispants, we show that acod1- and gpr84-deficient larvae are more susceptible to Shigella infection. Together, these results highlight the power of zebrafish to model infection by bacterial pathogens and reveal the mRNA expression of the early (acutely infected) and late (clearing) host response to Shigella infection.
  • Shigella Serotypes Associated with Carriage in Humans Establish Persistent Infection in Zebrafish
    Vincenzo Torraca, Dominik Brokatzky, Sydney L Miles, Charlotte E Chong, P Malaka De Silva, Stephen Baker, Claire Jenkins, Kathryn E Holt, Kate S Baker, Serge Mostowy
    Journal of Infectious Diseases, 2023
    Shigella represents a paraphyletic group of enteroinvasive Escherichia coli. More than 40 Shigella serotypes have been reported. However, most cases within the men who have sex with men (MSM) community are attributed to 3 serotypes: Shigella sonnei unique serotype and Shigella flexneri 2a and 3a serotypes. Using the zebrafish model, we demonstrate that Shigella can establish persistent infection in vivo. Bacteria are not cleared by the immune system and become antibiotic tolerant. Establishment of persistent infection depends on the O-antigen, a key constituent of the bacterial surface and a serotype determinant. Representative isolates associated with MSM transmission persist in zebrafish, while representative isolates of a serotype not associated with MSM transmission do not. Isolates of a Shigella serotype establishing persistent infections elicited significantly less macrophage death in vivo than isolates of a serotype unable to persist. We conclude that zebrafish are a valuable platform to illuminate factors underlying establishment of Shigella persistent infection in humans.
  • RUNDC1 inhibits autolysosome formation and survival of zebrafish via clasping ATG14-STX17-SNAP29 complex
    Rui Zhang, Yuyan Yang, Chao He, Xin Zhang, Vincenzo Torraca, Shen Wang, Nan Liu, Jiaren Yang, Shicheng Liu, Jinglei Yuan, Dongzhi Gou, Shi Li, Xueying Dong, Yufei Xie, Junling He, Hua Bai, Mengyu Hu, Zhiquan Liao, Yuan Huang, Hao Lyu, Shuai Xiao, Dong Guo, Declan William Ali, Marek Michalak, Cong Ma, Xing-Zhen Chen, Jingfeng Tang, Cefan Zhou
    Cell Death and Differentiation, 2023
  • Zebrafish null mutants of Sept6 and Sept15 are viable but more susceptible to Shigella infection
    Vincenzo Torraca, Magdalena K. Bielecka, Margarida C. Gomes, Dominik Brokatzky, Elisabeth M. Busch‐Nentwich, Serge Mostowy
    Cytoskeleton, 2023
  • Septins promote caspase activity and coordinate mitochondrial apoptosis
    Hoan Van Ngo, Stevens Robertin, Dominik Brokatzky, Magdalena K. Bielecka, Damián Lobato‐Márquez, Vincenzo Torraca, Serge Mostowy
    Cytoskeleton, 2023
  • P1 Bacteriophage-Enabled Delivery of CRISPR-Cas9 Antimicrobial Activity Against Shigella flexneri
    Yang W. Huan, Vincenzo Torraca, Russell Brown, Jidapha Fa-arun, Sydney L. Miles, Diego A. Oyarzún, Serge Mostowy, Baojun Wang
    ACS Synthetic Biology, 2023
  • Acquisition of a large virulence plasmid (pINV) promoted temperature-dependent virulence and global dispersal of O96:H19 enteroinvasive Escherichia coli
    Sydney L. Miles, Vincenzo Torraca, Zoe A. Dyson, Ana Teresa López-Jiménez, Ebenezer Foster-Nyarko, Damián Lobato-Márquez, Claire Jenkins, Kathryn E. Holt, Serge Mostowy
    Mbio, 2023
  • Editorial: Zebrafish Models for Human Disease Studies
    Liqing Zang, Vincenzo Torraca, Yasuhito Shimada, Norihiro Nishimura
    Frontiers in Cell and Developmental Biology, 2022
  • Editorial: Nucleic Acid-Associated Inflammation
    Nadine Laguette, Christelle Langevin, David Olagnier, Vincenzo Torraca, Claire Vanpouille-Box, Eloi R. Verrier
    Frontiers in Immunology, 2021
  • Disruption of Cxcr3 chemotactic signaling alters lysosomal function and renders macrophages more microbicidal
    Frida Sommer, Vincenzo Torraca, Yufei Xie, Aliede E. in ‘t Veld, Joost Willemse, Annemarie H. Meijer
    Cell Reports, 2021
  • In vivo biomolecular imaging of zebrafish embryos using confocal Raman spectroscopy
    Håkon Høgset, Conor C. Horgan, James P. K. Armstrong, Mads S. Bergholt, Vincenzo Torraca, Qu Chen, Timothy J. Keane, Laurence Bugeon, Margaret J. Dallman, Serge Mostowy, Molly M. Stevens
    Nature Communications, 2020
  • Shigella sonnei
    Vincenzo Torraca, Kathryn Holt, Serge Mostowy
    Trends in Microbiology, 2020
  • Deficiency in the autophagy modulator Dram1 exacerbates pyroptotic cell death of Mycobacteria-infected macrophages
    Rui Zhang, Monica Varela, Gabriel Forn-Cuní, Vincenzo Torraca, Michiel van der Vaart, Annemarie H. Meijer
    Cell Death and Disease, 2020
  • Chemokine Receptors and Phagocyte Biology in Zebrafish
    Frida Sommer, Vincenzo Torraca, Annemarie H. Meijer
    Frontiers in Immunology, 2020
  • Analysis tools to quantify dissemination of pathology in zebrafish larvae
    David R. Stirling, Oniz Suleyman, Eliza Gil, Philip M. Elks, Vincenzo Torraca, Mahdad Noursadeghi, Gillian S. Tomlinson
    Scientific Reports, 2020
  • Frontline Science: Antagonism between regular and atypical Cxcr3 receptors regulates macrophage migration during infection and injury in zebrafish
    Frida Sommer, Vincenzo Torraca, Sarah M. Kamel, Amber Lombardi, Annemarie H. Meijer
    Journal of Leukocyte Biology, 2020
  • Corrigendum: RNAseq Profiling of Leukocyte Populations in Zebrafish Larvae Reveals a cxcl11 Chemokine Gene as a Marker of Macrophage Polarization During Mycobacterial Infection (Frontiers in Immunology, (2019), 10, 10.3389/fimmu.2019.00832)
    Julien Rougeot, Vincenzo Torraca, Ania Zakrzewska, Zakia Kanwal, Hans J. Jansen, Frida Sommer, Herman P. Spaink, Annemarie H. Meijer
    Frontiers in Immunology, 2019
  • CXCR4 signaling regulates metastatic onset by controlling neutrophil motility and response to malignant cells
    C. Tulotta, C. Stefanescu, Q. Chen, V. Torraca, A. H. Meijer, B. E. Snaar-Jagalska
    Scientific Reports, 2019
  • Shigella sonnei o-antigen inhibits internalization, vacuole escape, and inflammasome activation
    Jayne L. Watson, Julia Sanchez-Garrido, Philippa J. Goddard, Vincenzo Torraca, Serge Mostowy, Avinash R. Shenoy, Abigail Clements
    Mbio, 2019
  • Meeting report: Zebrafish Infection and Immunity 2019
    Vincenzo Torraca, Margarida C. Gomes, Milka Sarris, Serge Mostowy
    Lab Animal, 2019
  • Macrophages target Salmonella by Lc3-associated phagocytosis in a systemic infection model
    Samrah Masud, Tomasz K. Prajsnar, Vincenzo Torraca, Gerda E.M. Lamers, Marianne Benning, Michiel Van Der Vaart, Annemarie H. Meijer
    Autophagy, 2019
  • RNAseq profiling of leukocyte populations in zebrafish larvae reveals a cxcl11 chemokine gene as a marker of macrophage polarization during mycobacterial infection
    Julien Rougeot, Vincenzo Torraca, Ania Zakrzewska, Zakia Kanwal, Hans J. Jansen, Frida Sommer, Herman P. Spaink, Annemarie H. Meijer
    Frontiers in Immunology, 2019
  • Shigella sonnei infection of zebrafish reveals that O-antigen mediates neutrophil tolerance and dysentery incidence
    Vincenzo Torraca, Myrsini Kaforou, Jayne Watson, Gina M. Duggan, Hazel Guerrero-Gutierrez, Sina Krokowski, Michael Hollinshead, Thomas B. Clarke, Rafal J. Mostowy, Gillian S. Tomlinson, Vanessa Sancho-Shimizu, Abigail Clements, Serge Mostowy
    Plos Pathogens, 2019
  • Shigella-induced emergency granulopoiesis protects Zebrafish Larvae from secondary infection
    Alexandra R. Willis, Vincenzo Torraca, Margarida C. Gomes, Jennifer Shelley, Maria Mazon-Moya, Alain Filloux, Cristina Lo Celso, Serge Mostowy
    Mbio, 2018
  • Zebrafish Infection: From Pathogenesis to Cell Biology
    Vincenzo Torraca, Serge Mostowy
    Trends in Cell Biology, 2018
  • Functional analysis reveals no transcriptional role for the glucocorticoid receptor β-isoform in zebrafish
    Antonia Chatzopoulou, Peter J. Schoonheim, Vincenzo Torraca, Annemarie H. Meijer, Herman P. Spaink, Marcel J.M. Schaaf
    Molecular and Cellular Endocrinology, 2017
  • The chemokine receptor CXCR4 promotes granuloma formation by sustaining a mycobacteria-induced angiogenesis programme
    Vincenzo Torraca, Claudia Tulotta, B. Ewa Snaar-Jagalska, Annemarie H. Meijer
    Scientific Reports, 2017
  • The inflammatory chemokine Cxcl18b exerts neutrophil-specific chemotaxis via the promiscuous chemokine receptor Cxcr2 in zebrafish
    Vincenzo Torraca, Natasja A. Otto, Aidin Tavakoli-Tameh, Annemarie H. Meijer
    Developmental and Comparative Immunology, 2017
  • Modeling Infectious Diseases in the Context of a Developing Immune System
    Samrah Masud, Vincenzo Torraca, Annemarie H. Meijer
    Current Topics in Developmental Biology, 2017
  • Septins restrict inflammation and protect zebrafish larvae from Shigella infection
    Maria J. Mazon-Moya, Alexandra R. Willis, Vincenzo Torraca, Laurent Boucontet, Avinash R. Shenoy, Emma Colucci-Guyon, Serge Mostowy
    Plos Pathogens, 2017
  • Septins and bacterial infection
    Vincenzo Torraca, Serge Mostowy
    Frontiers in Cell and Developmental Biology, 2016
  • The CXCR3-CXCL11 signaling axis mediates macrophage recruitment and dissemination of mycobacterial infection
    Vincenzo Torraca, Chao Cui, Ralf Boland, Jan-Paul Bebelman, Astrid M. van der Sar, Martine J. Smit, Marco Siderius, Herman P. Spaink, Annemarie H. Meijer
    Dmm Disease Models and Mechanisms, 2015
  • Macrophage-pathogen interactions in infectious diseases: New therapeutic insights from the zebrafish host model
    Vincenzo Torraca, Samrah Masud, Herman P. Spaink, Annemarie H. Meijer
    Dmm Disease Models and Mechanisms, 2014
  • Robotic injection of zebrafish embryos for high-throughput screening in disease models
    Herman P. Spaink, Chao Cui, Malgorzata I. Wiweger, Hans J. Jansen, Wouter J. Veneman, Rubén Marín-Juez, Jan de Sonneville, Anita Ordas, Vincenzo Torraca, Wietske van der Ent, William P. Leenders, Annemarie H. Meijer, B. Ewa Snaar-Jagalska, Ron P. Dirks
    Methods, 2013
  • Ultra-small graphene oxide functionalized with polyethylenimine (PEI) for very efficient gene delivery in cell and zebrafish embryos
    Xiang Zhou, Fabrice Laroche, Gerda E. M. Lamers, Vincenzo Torraca, Patrick Voskamp, Tao Lu, Fuqiang Chu, Herman P. Spaink, Jan Pieter Abrahams, Zunfeng Liu
    Nano Research, 2012

RECENT SCHOLAR PUBLICATIONS

  • Genome-wide analysis exploring mechanisms used by Shigella sonnei to survive long-term nutrient starvation
    XM Matanza, PB Leung, V Torraca, J Watson, MJ Dorman, NR Thomson, ...
    Msystems 11 (4), e00088-26 , 2026
    2026
  • Population structure, antimicrobial resistance, and virulence factors of diabetic foot-associated Escherichia coli
    V Ajumobi, Z Tahir, P Hayes, A McCormick, V Torraca
    Microbiology Spectrum, e02837-25 , 2026
    2026
  • A public resource of 15 genomically characterized representative strains of Shigella sonnei
    SL Miles, J Hawkey, B Vezina, V Torraca, C Jenkins, FX Weill, S Baker, ...
    Microbial genomics 12 (1), 001596 , 2026
    2026
    Citations: 4
  • VAMP8 stabilization by DRAM1 enables autophagosome-lysosome fusion and promotes metastatic extravasation
    R Zhang, V Torraca, C Yan, H Lyu, S Xiao, D Guo, Q Zhang, C Zhou, ...
    Autophagy 21 (11), 2531-2533 , 2025
    2025
    Citations: 2
  • Enhanced virulence and stress tolerance are signatures of epidemiologically successful Shigella sonnei
    SL Miles, D Santillo, H Painter, K Wright, V Torraca, AT López-Jiménez, ...
    Nature communications 16 (1), 9005 , 2025
    2025
    Citations: 6
  • DRAM1 promotes the stability of lysosomal VAMP8 to enhance autolysosome formation and facilitates the extravasation
    R Zhang, X Zhang, H Bai, Q Cheng, X Yao, S Li, V Torraca, C Yan, ...
    Nature communications 16 (1), 5826 , 2025
    2025
    Citations: 10
  • Clinical microbiology in the genomic era
    V Torraca
    Medical Genetics and Genomics, 384 , 2025
    2025
  • Doctoral supervision training in the UK: Themes and design elements of structured training programmes
    V Torraca
    2025
  • ILKAP promotes the metastasis of hepatocellular carcinoma cells by inhibiting β‐catenin degradation and enhancing the WNT signaling pathway
    R Zhang, J Yuan, S Liu, V Torraca, Z Liao, Y Wu, H Tan, X Yao, X Hou, ...
    Advanced biology 8 (5), 2300117 , 2024
    2024
    Citations: 2
  • RUNDC1 negatively mediates the fusion of autophagosomes with lysosomes via regulating SNARE complex assembly
    R Zhang, V Torraca, H Lyu, S Xiao, D Guo, C Zhou, J Tang
    Autophagy 20 (2), 454-456 , 2024
    2024
    Citations: 6
  • First person: Vincenzo Torraca
    V Torraca
    Disease Models and Mechanisms 17 (1) , 2024
    2024
  • Transcriptional profiling of zebrafish identifies host factors controlling susceptibility to Shigella flexneri
    V Torraca, RJ White, IM Sealy, M Mazon-Moya, G Duggan, AR Willis, ...
    Disease models & mechanisms 17 (1), dmm050431 , 2024
    2024
    Citations: 4
  • RUNDC1 inhibits autolysosome formation and survival of zebrafish via clasping ATG14-STX17-SNAP29 complex
    R Zhang, Y Yang, C He, X Zhang, V Torraca, S Wang, N Liu, J Yang, S Liu, ...
    Cell Death & Differentiation 30 (10), 2231-2248 , 2023
    2023
    Citations: 20
  • Acquisition of a large virulence plasmid (pINV) promoted temperature-dependent virulence and global dispersal of O96:H19 enteroinvasive Escherichia coli
    SL Miles, V Torraca, ZA Dyson, AT López-Jiménez, E Foster-Nyarko, ...
    Mbio 14 (4), e00882-23 , 2023
    2023
    Citations: 11
  • Zebrafish null mutants of Sept6 and Sept15 are viable but more susceptible to Shigella infection
    V Torraca, MK Bielecka, MC Gomes, D Brokatzky, EM Busch‐Nentwich, ...
    Cytoskeleton 80 (7-8), 266-274 , 2023
    2023
    Citations: 10
  • Septins promote caspase activity and coordinate mitochondrial apoptosis
    H Van Ngo, S Robertin, D Brokatzky, MK Bielecka, D Lobato‐Márquez, ...
    Cytoskeleton 80 (7-8), 254-265 , 2023
    2023
    Citations: 15
  • P1 Bacteriophage-Enabled Delivery of CRISPR-Cas9 Antimicrobial Activity Against Shigella flexneri
    YW Huan, V Torraca, R Brown, J Fa-Arun, SL Miles, DA Oyarzún, ...
    ACS synthetic biology 12 (3), 709-721 , 2023
    2023
    Citations: 41
  • Major Article: Shigella serotypes associated with carriage in humans establish persistent infection in zebrafish
    V Torraca, D Brokatzky, SL Miles, CE Chong, PM De Silva, S Baker, ...
    2023
    Citations: 16
  • Zebrafish models for human disease studies
    L Zang, V Torraca, Y Shimada, N Nishimura
    Frontiers in Cell and Developmental Biology 10, 861941 , 2022
    2022
    Citations: 27
  • Editorial: Nucleic acid-associated inflammation
    N Laguette, C Langevin, D Olagnier, V Torraca, C Vanpouille-Box, ...
    Front. Immunol. 12: 791580. doi: 10.3389/fimmu , 2021
    2021

MOST CITED SCHOLAR PUBLICATIONS

  • Zebrafish infection: From pathogenesis to cell biology
    V Torraca, S Mostowy
    Trends in cell biology 28 (2), 143-156 , 2018
    2018
    Citations: 209
  • Macrophage-pathogen interactions in infectious diseases: new therapeutic insights from the zebrafish host model
    V Torraca, S Masud, HP Spaink, AH Meijer
    Disease models & mechanisms 7 (7), 785-797 , 2014
    2014
    Citations: 198
  • The CXCR3-CXCL11 signaling axis mediates macrophage recruitment and dissemination of mycobacterial infection
    V Torraca, C Cui, R Boland, JP Bebelman, AM Van Der Sar, MJ Smit, ...
    Disease models & mechanisms 8 (3), 253-269 , 2015
    2015
    Citations: 165
  • Robotic injection of zebrafish embryos for high-throughput screening in disease models
    HP Spaink, C Cui, MI Wiweger, HJ Jansen, WJ Veneman, R Marín-Juez, ...
    Methods 62 (3), 246-254 , 2013
    2013
    Citations: 140
  • Macrophages target Salmonella by Lc3-associated phagocytosis in a systemic infection model
    S Masud, TK Prajsnar, V Torraca, GEM Lamers, M Benning, ...
    Autophagy 15 (5), 796-812 , 2019
    2019
    Citations: 129
  • RNAseq Profiling of Leukocyte Populations in Zebrafish Larvae Reveals a cxcl11 Chemokine Gene as a Marker of Macrophage Polarization During Mycobacterial …
    J Rougeot, V Torraca, A Zakrzewska, Z Kanwal, HJ Jansen, F Sommer, ...
    Frontiers in immunology 10, 832 , 2019
    2019
    Citations: 115
  • Ultra-small graphene oxide functionalized with polyethylenimine (PEI) for very efficient gene delivery in cell and zebrafish embryos
    X Zhou, F Laroche, GEM Lamers, V Torraca, P Voskamp, T Lu, F Chu, ...
    Nano Research 5 (10), 703-709 , 2012
    2012
    Citations: 99
  • In vivo biomolecular imaging of zebrafish embryos using confocal Raman spectroscopy
    H Høgset, CC Horgan, JPK Armstrong, MS Bergholt, V Torraca, Q Chen, ...
    Nature Communications 11 (1), 6172 , 2020
    2020
    Citations: 93
  • CXCR4 signaling regulates metastatic onset by controlling neutrophil motility and response to malignant cells
    C Tulotta, C Stefanescu, Q Chen, V Torraca, AH Meijer, ...
    Scientific reports 9 (1), 2399 , 2019
    2019
    Citations: 92
  • Modeling infectious diseases in the context of a developing immune system
    S Masud, V Torraca, AH Meijer
    Current topics in developmental biology 124, 277-329 , 2017
    2017
    Citations: 77
  • Septins restrict inflammation and protect zebrafish larvae from Shigella infection
    MJ Mazon-Moya, AR Willis, V Torraca, L Boucontet, AR Shenoy, ...
    PLoS pathogens 13 (6), e1006467 , 2017
    2017
    Citations: 70
  • The inflammatory chemokine Cxcl18b exerts neutrophil-specific chemotaxis via the promiscuous chemokine receptor Cxcr2 in zebrafish
    V Torraca, NA Otto, A Tavakoli-Tameh, AH Meijer
    Developmental & Comparative Immunology 67, 57-65 , 2017
    2017
    Citations: 65
  • Septins and bacterial infection
    V Torraca, S Mostowy
    Frontiers in cell and developmental biology 4, 127 , 2016
    2016
    Citations: 63
  • Chemokine receptors and phagocyte biology in zebrafish
    F Sommer, V Torraca, AH Meijer
    Frontiers in immunology 11, 325 , 2020
    2020
    Citations: 62
  • Deficiency in the autophagy modulator Dram1 exacerbates pyroptotic cell death of Mycobacteria-infected macrophages
    R Zhang, M Varela, G Forn-Cuní, V Torraca, M van der Vaart, AH Meijer
    Cell death & disease 11 (4), 277 , 2020
    2020
    Citations: 60
  • Shigella sonnei
    V Torraca, K Holt, S Mostowy
    Trends in microbiology 28 (8), 696-697 , 2020
    2020
    Citations: 53
  • P1 Bacteriophage-Enabled Delivery of CRISPR-Cas9 Antimicrobial Activity Against Shigella flexneri
    YW Huan, V Torraca, R Brown, J Fa-Arun, SL Miles, DA Oyarzún, ...
    ACS synthetic biology 12 (3), 709-721 , 2023
    2023
    Citations: 41
  • The chemokine receptor CXCR4 promotes granuloma formation by sustaining a mycobacteria-induced angiogenesis programme
    V Torraca, C Tulotta, BE Snaar-Jagalska, AH Meijer
    Scientific reports 7 (1), 45061 , 2017
    2017
    Citations: 41
  • Frontline science: Antagonism between regular and atypical Cxcr3 receptors regulates macrophage migration during infection and injury in zebrafish
    F Sommer, V Torraca, SM Kamel, A Lombardi, AH Meijer
    Journal of leukocyte biology 107 (2), 185-203 , 2020
    2020
    Citations: 40
  • Shigella sonnei O-Antigen Inhibits Internalization, Vacuole Escape, and Inflammasome Activation
    JL Watson, J Sanchez-Garrido, PJ Goddard, V Torraca, S Mostowy, ...
    MBio 10 (6), 10.1128/mbio. 02654-19 , 2019
    2019
    Citations: 39