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Autophagy Receptor Tollip Facilitates Bacterial Autophagy by Recruiting Galectin-7 in Response to Group A Streptococcus Infection
- Source :
- Frontiers in Cellular and Infection Microbiology, Vol 10 (2020)
- Publication Year :
- 2020
- Publisher :
- Frontiers Media S.A., 2020.
-
Abstract
- Bacterial autophagy—a type of macroautophagy that is also termed xenophagy—selectively targets intracellular bacteria such as group A Streptococcus (GAS), a ubiquitous pathogen that causes numerous serious diseases, including pharyngitis, skin infections, and invasive life-threatening infections. Although bacterial autophagy is known to eliminate invading bacteria via the action of autophagy receptors, the underlying mechanism remains unclear. Herein, we elucidated that Tollip functions as a bacterial-autophagy receptor in addition to participating involved in the intracellular immunity mechanism that defends against bacterial infection. Tollip was recruited to GAS-containing endosomal vacuoles prior to the escape of GAS into the cytosol; additionally, Tollip knockout disrupted the recruitment of other autophagy receptors, such as NBR1, TAX1BP1, and NDP52, to GAS-containing autophagosomes and led to prolonged intracellular survival of GAS. Furthermore, Tollip was found to be required for the recruitment of galectin-1 and -7 to GAS-containing autophagosomes, and immunoprecipitation results indicated that Tollip interacts with galectin-7. Lastly, our data also revealed that galectin-1 and -7 are involved in the restriction of GAS replication in cells. These results demonstrated that Tollip modulates bacterial autophagy by recruiting other autophagy receptors and galectins.
- Subjects :
- tollip
autophagy
group A Streptoccocus
galectin 7
galectin 1
Microbiology
QR1-502
Subjects
Details
- Language :
- English
- ISSN :
- 22352988
- Volume :
- 10
- Database :
- Directory of Open Access Journals
- Journal :
- Frontiers in Cellular and Infection Microbiology
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.0f7fd3f591fc464593cb41e78161c281
- Document Type :
- article
- Full Text :
- https://doi.org/10.3389/fcimb.2020.583137