Description:

Microbiology-Immunology Seminar Series

Intracellular bacterial pathogens such as Legionella, Chlamydia and Brucella can subvert the function of the host cell’s early secretory pathway to replicate within a membrane-bound compartment associated with the endoplasmic reticulum. To test the hypothesis that this shared pathogenic strategy of parasitizing secretory pathway function is a pattern of pathogenesis detected by the host’s innate immune system, we utilized the zoonotic pathogen Brucella abortus, which employs a Type IV secretion (T4SS) to subvert the secretory pathway. The T4SS effector VceC elicits inflammation by activating the IRE1 signaling pathway of the unfolded protein response (UPR). The link between IRE1 activation and activation of NF-kB and IL-6 production during bacterial infection required NOD1 and NOD2, two members of the NLR family of pattern recognition receptors. These findings may help to understand the involvement of NOD proteins in inflammatory responses to viral infection as well as in pathologic responses such as inflammatory bowel disease that have an ER stress component.

Renee Tsolis, PhD

University of California at Davis

Host: Nicholas Cianciotto, PhD