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Updated: May 25, 2026
11:10
High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
Published on: August 11, 2014
A novel contractility pathway operating in Salmonella invasion.
Jan Hänisch1, Theresia E B Stradal, Klemens Rottner
1Helmholtz Centre for Infection Research, Braunschweig, Germany.
Virulence
|January 31, 2012
Summary
Salmonella typhimurium invasion uses a novel mechanism, hijacking host cell contraction via myosin II and RhoA/ROCK signaling, independent of membrane ruffling and Arp2/3 complex.
Area of Science:
- Cellular microbiology
- Bacterial pathogenesis
- Host-pathogen interactions
Background:
- Salmonella typhimurium employs diverse invasion strategies into host cells.
- The canonical "trigger" mechanism involves membrane ruffling and macropinocytosis.
- A novel, ruffling-independent invasion pathway has recently been identified.
Purpose of the Study:
- To elucidate the mechanism of Salmonella's contraction-dependent host cell entry.
- To identify bacterial and host factors involved in this novel invasion pathway.
- To discuss implications for bacterial pathogen entry and classification.
Main Methods:
- Investigation of host cell contraction machinery during Salmonella invasion.
- Analysis of RhoA/Rho-kinase signaling pathway activation.
- Assessment of the role of Salmonella virulence factor SopB.
- Evaluation of Arp2/3 complex independence.
Main Results:
- Salmonella invasion utilizes a contraction-dependent mechanism involving myosin II-rich structures.
- This pathway is stimulated by RhoA/Rho-kinase signaling, downstream of SopB.
- The mechanism operates independently of the Arp2/3 complex, unlike macropinocytosis.
Conclusions:
- A novel, contraction-based Salmonella invasion mechanism exists alongside the trigger mode.
- This pathway offers new insights into bacterial entry strategies.
- Findings may impact the classification of bacterial pathogen invasion mechanisms.
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