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Shigella effector IpaH9.8 binds to a splicing factor U2AF(35) to modulate host immune responses
Jun Okuda1, Takahito Toyotome, Naoyuki Kataoka
1Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8039, Japan.
Biochemical and Biophysical Research Communications
|June 14, 2005
Summary
Shigella
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Shigella employs type III secretion system (T3SS) effectors to manipulate host cells during infection.
- Modulation of host inflammatory responses is crucial for pathogen survival and virulence.
Purpose of the Study:
- To investigate the role of Shigella effector IpaH9.8 in modulating host inflammatory responses.
- To elucidate the molecular mechanism by which IpaH9.8 influences host cell processes and bacterial colonization.
Main Methods:
- Murine lung infection model to assess inflammatory responses and bacterial colonization.
- Binding assays to identify host targets of IpaH9.8.
- RNA analysis (RT-PCR) to evaluate gene expression changes in host cells.
Main Results:
- A DeltaipaH9.8 mutant induced more severe inflammation and pro-inflammatory cytokine production in vivo.
- IpaH9.8 specifically binds to the mammalian splicing factor U2AF(35), inhibiting U2AF(35)-dependent splicing.
- Reduced U2AF(35) levels led to decreased expression of key inflammatory genes (il-8, RANTES, GM-CSF, il-1beta) in host cells.
Conclusions:
- IpaH9.8 optimizes host inflammatory responses during Shigella infection.
- This modulation by IpaH9.8 facilitates bacterial colonization within host epithelial cells.