ArticlePLoS pathogens2009
The Salmonella SPI2 effector SseI mediates long-term systemic infection by modulating host cell migration.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
79 citing papers in PubMed, 139 citations in OpenAlex.
- Host-microbiota-pathogen interactions drive Salmonella enterica serovar Typhimurium pathogenesis.Nature reviews. Microbiology · 2026Review
- The Manipulation of Host Cells byInternational journal of molecular sciences · 2026Review
- The interplay betweenCell insight · 2025Review
- Review
- Genomic characterization of antimicrobial-resistantFrontiers in microbiology · 2025Article
- A pan-genome perspective on the evolutionary dynamics of polyphyly, virulence, and antibiotic resistance inCurrent research in food science · 2025Article
- Infection biology ofEcoSal Plus · 2024Review
- Fighting the enemy within: Systemic immune defense against mucosal Salmonella infection.Immunology letters · 2024Review
- Critical role ofApplied and environmental microbiology · 2024Article
- Salmonella manipulates macrophage migration via SteC-mediated myosin light chain activation to penetrate the gut-vascular barrier.The EMBO journal · 2024Article
- Dynamics of macrophage polarization supporteLife · 2024Article
- Molecular Characteristics ofInfection and drug resistance · 2024Article
- Review
- Clinical Characteristics, Antimicrobial Resistance, Virulence Genes and Multi-Locus Sequence Typing of Non-TyphoidalMicroorganisms · 2023Article
- Speaking the host language: howMicrobiology (Reading, England) · 2023Review
- The thin line between conventional dendritic cells (cDCs) and group 3 innate lymphoid cells (ILC3s) in the gut.International immunology · 2023Article
- Manipulation of host immune defenses by effector proteins delivered from multiple secretion systems ofFrontiers in immunology · 2023Review
- Mechanical Forces Govern Interactions of Host Cells with Intracellular Bacterial Pathogens.Microbiology and molecular biology reviews : MMBR · 2022Review
- Article
- Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Host-adapted strains of Salmonella enterica cause systemic infections and have the ability to persist systemically for long periods of time despite the presence of a robust immune response. Chronically infected hosts are asymptomatic and transmit disease to naïve hosts via fecal shedding of bacteria, thereby serving as a critical reservoir for disease. We show that the bacterial effector protein SseI (also called SrfH), which is translocated into host cells by the Salmonella Pathogenicity Island 2 (SPI2) type III secretion system (T3SS), is required for Salmonella typhimurium to maintain a long-term chronic systemic infection in mice. SseI inhibits normal cell migration of primary macrophages and dendritic cells (DC) in vitro, and such inhibition requires the host factor IQ motif containing GTPase activating protein 1 (IQGAP1), an important regulator of cell migration. SseI binds directly to IQGAP1 and co-localizes with this factor at the cell periphery. The C-terminal domain of SseI is similar to PMT/ToxA, a bacterial toxin that contains a cysteine residue (C1165) that is critical for activity. Mutation of the corresponding residue in SseI (C178A) eliminates SseI function in vitro and in vivo, but not binding to IQGAP1. In addition, infection with wild-type (WT) S. typhimurium suppressed DC migration to the spleen in vivo in an SseI-dependent manner. Correspondingly, examination of spleens from mice infected with WT S. typhimurium revealed fewer DC and CD4(+) T lymphocytes compared to mice infected with Delta sseI S. typhimurium. Taken together, our results demonstrate that SseI inhibits normal host cell migration, which ultimately counteracts the ability of the host to clear systemic bacteria.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.