Journal
AUTOPHAGY
Volume 11, Issue 7, Pages 1184-1186Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2015.1058685
Keywords
ADAM10; ATG16L1; Staphylococcus aureus; tolerance; alpha-toxin
Categories
Funding
- US National Institute of Health (NIH) [R01 DK093668, T32 GM0738, AI100853, F30 DK098925, R01AI099394, R01AI105129]
- American Heart Association [12GRNT12030041]
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Defense strategies against infectious threats can be divided into resistance and tolerance mechanisms. Resistance mechanisms involve reduction of pathogen burden and include many established examples, one of them being the destruction of intracellular pathogens through autophagy (xenophagy). Tolerance mechanisms protect the host from damage caused by the pathogen or the immune response independent of pathogen load. The role of autophagy in maintaining homeostasis in response to environmental stress suggests that this pathway is involved in tolerance to a variety of infectious agents. However, demonstrating that autophagy promotes tolerance independent of its role in resistance has been a challenge, especially during infection by clinically relevant pathogens. We have found that autophagy protects against Staphylococcus aureus infection by maintaining tolerance toward a pore forming toxin secreted by the bacteria, -toxin.
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