IsaB Inhibits Autophagic Flux to Promote Host Transmission of Methicillin-Resistant Staphylococcus aureus

Pei Feng Liu, Jin Shiung Cheng, Cheng Len Sy, Wei Chun Huang, Hsiu Chen Yang, Richard L. Gallo, Chun Ming Huang, Chih Wen Shu

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

Methicillin-resistant Staphylococcus aureus (MRSA) has emerged as a major nosocomial pathogen that is widespread in both health-care facilities and in the community at large, as a result of direct host-to-host transmission. Several virulence factors are associated with pathogen transmission to naive hosts. Immunodominant surface antigen B (IsaB) is a virulence factor that helps Staphylococcus aureus to evade the host defense system. However, the mechanism of IsaB on host transmissibility remains unclear. We found that IsaB expression was elevated in transmissible MRSA. Wild-type isaB strains inhibited autophagic flux to promote bacterial survival and elicit inflammation in THP-1 cells and mouse skin. MRSA isolates with increased IsaB expression showed decreased autophagic flux, and the MRSA isolate with the lowest IsaB expression showed increased autophagic flux. In addition, recombinant IsaB rescued the virulence of the isaB deletion strain and increased the group A streptococcus (GAS) virulence in vivo. Together, these results reveal that IsaB diminishes autophagic flux, thereby allowing MRSA to evade host degradation. These findings suggest that IsaB is a suitable target for preventing or treating MRSA infection.

Original languageEnglish
Pages (from-to)2714-2722
Number of pages9
JournalJournal of Investigative Dermatology
Volume135
Issue number11
DOIs
StatePublished - 1 Nov 2015

Fingerprint

Dive into the research topics of 'IsaB Inhibits Autophagic Flux to Promote Host Transmission of Methicillin-Resistant Staphylococcus aureus'. Together they form a unique fingerprint.

Cite this