Loading...
Stress-induced host membrane remodeling protects from infection by non-motile bacterial pathogens.
Tawk, Caroline Nigro, Giulia Rodrigues Lopes, Ines Aguilar, Carmen Lisowski, Clivia Mano, Miguel Sansonetti, Philippe
Tawk, Caroline
Nigro, Giulia
Rodrigues Lopes, Ines
Aguilar, Carmen
Lisowski, Clivia
Mano, Miguel
Sansonetti, Philippe
Citations
Altmetric:
Advisors
Editors
Other Contributors
Issue Date
2018-11-02
Submitted date
Files
Loading...
original manuscript
Adobe PDF, 415.12 KB
Loading...
all figures
Adobe PDF, 3.02 MB
Other Titles
Abstract
While mucosal inflammation is a major source of stress during enteropathogen infection, it remains to be fully elucidated how the host benefits from this environment to clear the pathogen. Here, we show that host stress induced by different stimuli mimicking inflammatory conditions strongly reduces the binding of Shigella flexneri to epithelial cells. Mechanistically, stress activates acid sphingomyelinase leading to host membrane remodeling. Consequently, knockdown or pharmacological inhibition of the acid sphingomyelinase blunts the stress-dependent inhibition of Shigella binding to host cells. Interestingly, stress caused by intracellular Shigella replication also results in remodeling of the host cell membrane, in vitro and in vivo, which precludes re-infection by this and other non-motile pathogens. In contrast, Salmonella Typhimurium overcomes the shortage of permissive entry sites by gathering effectively at the remaining platforms through its flagellar motility. Overall, our findings reveal host membrane remodeling as a novel stress-responsive cell-autonomous defense mechanism that protects epithelial cells from infection by non-motile bacterial pathogens.
Citation
Publisher
Journal
PubMed ID
PubMed Central ID
Additional Links
Embedded video
Type
Article
Language
Description
Series/Report no.
ISSN
1460-2075
EISSN
ISBN
ISMN
Gov't Doc #
Sponsors
License
Attribution-NonCommercial-ShareAlike 4.0 International