PeRsistent Infection of Shigella in Macrophages (PRISM): Shedding light on the intra-phagocytic lifestyle of Shigella sonnei using human induced pluripotent stem cell-derived macrophages
- Funded by European Commission
- Total publications:0 publications
Grant number: 101268479
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Key facts
Disease
ShigellosisStart & end year
20262028Known Financial Commitments (USD)
$299,400.11Funder
European CommissionPrincipal Investigator
Vincenzo TORRACAResearch Location
United KingdomLead Research Institution
KING'S COLLEGE LONDONResearch Priority Alignment
N/A
Research Category
Pathogen: natural history, transmission and diagnosticsResearch Subcategory
Pathogen morphology, shedding & natural historySpecial Interest Tags
N/AStudy Type
Non-ClinicalClinical Trial Details
N/ABroad Policy Alignment
PendingAge Group
Not ApplicableVulnerable Population
Not applicableOccupations of Interest
Not applicable
Abstract
Shigella is a human-adapted invasive pathogen and a high-priority antimicrobial resistance (AMR) threat, responsible for up to 165 million cases of bacillary dysentery and over 200,000 deaths annually. Emerging evidence shows that certain lineages of Shigella, including Shigella sonnei, can establish long-term infections in patients and animal models. Persistent infections are a significant public health threat, as they can cause recurrent disease manifestations. Persistent infections also complicate diagnosis, encourage transmission, and reduce the effectiveness of antibiotic treatments, promoting the emergence of AMR. My findings reveal that S. sonnei can survive within human macrophages, challenging the long-standing view that Shigella invariably induces rapid macrophage death. The S. sonnei O-antigen, a surface polysaccharide, contributes significantly to the establishment of persistent infections; however, the exact mechanisms by which S. sonnei persists remain unknown. Using infections of human-induced pluripotent stem cell-derived macrophages, I aim to (i) characterise the S. sonnei intra-macrophage persistent infection niche (I will identify where and how S. sonnei survives inside macrophages, and which host pathways are altered during long-term infection); and (ii) dissect the role of the O-antigen in promoting persistent infection (I will determine how the O-antigen affects bacterial survival in host macrophages and how it contributes to immune evasion). To meet these objectives, I will adopt a multidisciplinary approach, involving stem cell technologies, advanced imaging techniques, state-of-the-art gene expression profiling, gene knockout-based screenings, and targeted modification of bacterial surface polysaccharides. This project will deliver the first characterisation of persistent S. sonnei infection in macrophages, shedding light on the development of improved diagnostics, therapeutics, and prophylactic strategies to combat Shigella infections.