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Cellular invasion by Staphylococcus aureus involves a fibronectin bridge between the bacterial fibronectin-binding
1Center for Extracellular Matrix Biology, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston 77030, USA.
European Journal of Cell Biology
|November 23, 2000
Summary
Staphylococcus aureus invasion into host cells requires bacterial fibronectin-binding proteins (FnBPs) and host cell beta1 integrins. These components form a bridge, facilitating bacterial uptake and cellular entry.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- Staphylococcus aureus is typically extracellular but can invade non-phagocytic cells.
- Bacterial surface proteins mediate host cell interactions.
Purpose of the Study:
- Investigate early stages of S. aureus cellular invasion.
- Identify bacterial and host factors essential for invasion.
Main Methods:
- Utilized S. aureus mutants lacking fibronectin-binding proteins (FnBPs).
- Assessed invasion using mouse fibroblast cell lines with and without beta1 integrin expression.
- Employed soluble recombinant FnBPs and anti-fibronectin antibodies to inhibit invasion.
Main Results:
- FnBP expression on S. aureus is crucial for efficient host cell uptake.
- Host cell fibronectin (FN) and beta1 integrins are essential for invasion.
- A model proposed FN bridging bacterial FnBPs and host beta1 integrins.
Conclusions:
- S. aureus invasion mechanism involves bacterial FnBPs and host beta1 integrins.
- FN acts as a molecular bridge in this interaction.
- Understanding this pathway can inform strategies against S. aureus infections.