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May 9, 2019 | 11:00 a.m. - 12:00 p.m.
Category: Seminar
Location: Scott Hall #3125 | Map
540 E. Canfield
Detroit, MI 48201
Cost: Free
Audience: Current Graduate Students, Faculty

Mary O’Riordan, PhD

Frederick C. Neidhardt Collegiate Professor of Microbiology & Immunology and Associate Dean of Graduate & Postdoctoral Studies, University of Michigan Medical School

"Cells on Fire – how Cellular Stress Shapes Innate Immune Defenses” 


Infection by pathogenic bacteria results in perturbation of host macrophages, leading to activation of cellular stress responses. Our previous studies have demonstrated a profound impact of endoplasmic reticulum stress on shaping the host inflammatory response. Most notably, the ER stress sensor IRE1 plays a key role in programming mitochondrial reactive oxygen species (ROS) production and mitochondrial damage. Although mitochondria-derived antimicrobial effectors like reactive oxygen species (mROS) aid in bacterial killing, it is unclear how these effectors reach bacteria within the phagosomal lumen. We find that IRE1 triggered upon methicillin-resistant Staphylococcus aureus (MRSA) infection induces mitochondrial peroxide that is delivered to bacteria-containing phagosomes via mitochondria-derived vesicles (MDVs). Accumulation of phagosomal H2O2 required Toll-like Receptor signaling and the mitochondrial superoxide dismutase (Sod2), which was found in MDVs. Sod2 depletion compromised mH2O2 production and bacterial killing. In addition to its central role in governing stress and inflammation in macrophages, we find that IRE1 is required for neutrophil defenses, including production of IL1-beta and anti-microbial neutrophil extracellular traps.

For more information about this event, please contact Suzanne Shaw at 5775325 or