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Published on: September 8, 2021
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The adherens junctions control susceptibility to Staphylococcus aureus α-toxin
Lauren M Popov1, Caleb D Marceau1, Philipp M Starkl2
1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305;
Summary
Plekstrin-homology domain containing protein 7 (PLEKHA7) controls Staphylococcus aureus alpha-toxin severity. This adherens junction protein
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- Staphylococcus aureus is a major human pathogen causing skin and lung infections.
- Alpha-toxin is a key virulence factor for S. aureus epithelial diseases.
Purpose of the Study:
- Identify host cellular factors involved in alpha-toxin cytotoxicity.
- Investigate the role of PLEKHA7 and adherens junctions in S. aureus infections.
Main Methods:
- Conducted a genetic screen using mutagenized haploid human cells.
- Utilized PLEKHA7 knockout cells and mice for infection studies.
- Infected mice with methicillin-resistant S. aureus USA300 LAC strain.
Main Results:
- PLEKHA7 was identified as a significant factor in alpha-toxin cytotoxicity.
- PLEKHA7 knockout cells showed recovery after alpha-toxin injury.
- PLEKHA7 deficiency reduced disease severity in mouse models of skin and pneumonia infections.
Conclusions:
- Adherens junctions, including PLEKHA7, actively regulate cellular responses to S. aureus alpha-toxin.
- PLEKHA7 plays a critical role in controlling S. aureus virulence and disease progression.
- PLEKHA7 is a potential therapeutic target to mitigate S. aureus epithelial infections.
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