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Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
The Salmonella SPI2 effector SseI mediates long-term systemic infection by modulating host cell migration
Laura M McLaughlin1, Gregory R Govoni, Christiane Gerke
1Department of Microbiology and Immunology, Stanford University Medical Center, Stanford, California, United States of America.
Plos Pathogens
|December 4, 2009
Summary
The bacterial effector protein SseI is crucial for Salmonella typhimurium to establish chronic systemic infections by inhibiting host cell migration. This protein interferes with macrophage and dendritic cell movement, aiding bacterial persistence.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Salmonella enterica causes persistent systemic infections in hosts.
- Chronic infections are asymptomatic and serve as disease reservoirs.
- The Salmonella Pathogenicity Island 2 (SPI2) type III secretion system (T3SS) delivers effector proteins into host cells.
Purpose of the Study:
- To investigate the role of the bacterial effector protein SseI in Salmonella typhimurium chronic systemic infections.
- To elucidate the mechanism by which SseI contributes to bacterial persistence.
Main Methods:
- Investigated the function of SseI in Salmonella typhimurium infection models in mice.
- Utilized in vitro assays to study the interaction between SseI and host cell factors.
- Employed genetic mutations to assess the importance of specific SseI residues and domains.
Main Results:
- SseI is essential for Salmonella typhimurium to maintain long-term chronic systemic infection in mice.
- SseI inhibits the migration of primary macrophages and dendritic cells by interacting with IQGAP1.
- A critical cysteine residue (C178A) in SseI is necessary for its function in vitro and in vivo.
- Wild-type S. typhimurium infection suppressed dendritic cell migration to the spleen in an SseI-dependent manner.
Conclusions:
- SseI plays a critical role in Salmonella typhimurium pathogenesis by inhibiting host cell migration.
- The interaction of SseI with IQGAP1 is key to its function in disrupting immune cell movement.
- SseI contributes to bacterial persistence by counteracting the host's ability to clear systemic infections.
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