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Suppression of starvation-induced autophagy by recombinant toxic shock syndrome toxin-1 in epithelial cells.

ABSTRACT: Toxic shock syndrome toxin-1 (TSST-1), a superantigen produced from Staphylococcus aureus, has been reported to bind directly to unknown receptor(s) and penetrate into non-immune cells but its function is unclear. In this study, we demonstrated that recombinant TSST-1 suppresses autophagosomal accumulation in the autophagic-induced HeLa 229 cells. This suppression is shared by a superantigenic-deficient mutant of TSST-1 but not by staphylococcal enterotoxins, suggesting that autophagic suppression of TSST-1 is superantigenic-independent. Furthermore, we showed that TSST-1-producing S. aureus suppresses autophagy in the response of infected cells. Our data provides a novel function of TSST-1 in autophagic suppression which may contribute in staphylococcal persistence in host cells.

SUBMITTER: Asano K

PROVIDER: S-EPMC4234639 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Suppression of starvation-induced autophagy by recombinant toxic shock syndrome toxin-1 in epithelial cells.

Asano Krisana K Asano Yoshiya Y Ono Hisaya K HK Nakane Akio A

PloS one 20141117 11

Toxic shock syndrome toxin-1 (TSST-1), a superantigen produced from Staphylococcus aureus, has been reported to bind directly to unknown receptor(s) and penetrate into non-immune cells but its function is unclear. In this study, we demonstrated that recombinant TSST-1 suppresses autophagosomal accumulation in the autophagic-induced HeLa 229 cells. This suppression is shared by a superantigenic-deficient mutant of TSST-1 but not by staphylococcal enterotoxins, suggesting that autophagic suppressi ...[more]

PMID: 25402468

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