Journal
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
Volume 10, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcimb.2020.583137
Keywords
tollip; autophagy; group A Streptoccocus; galectin 7; galectin 1
Categories
Funding
- Research Program on Emerging and Re-emerging Infectious Diseases [18fk0108044h0202, 18fk0108073h0001]
- J-PRIDE from Japan Agency for Medical Research and Development, AMED [18fm0208030h0002]
- Takeda Science Foundation
- [16H05188]
- [15K15130]
- [26462776]
- [17K19552]
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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.
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