Fig. 2.

Mechanisms of bacteria inducing UPR. (A) Grp94 chaperones TLR4 which is activated by binding of LPS. Under LPS stimulus, TLR4 is endocytosed and its expression is increased. In addition, the expression of grp94 is increased with a much lower magnitude than that of tlr4 resulting in accumulation of unfolded TLR4 within the ER. (B) PFTs induce ROS production, MAPK activation, and Ca²⁺ influx as well as induction of ER Ca²⁺ release resulting in UPR activation. (C) P. aeruginosa and bacterial-produced H₂O₂ induce UPR by MAPK activation and increase of ROS. (D) Tunicamycin inhibits N-glycosylation of proteins. (E) AB₅ toxins are endocytosed and transported via the Golgi apparatus to the ER where they induce UPR activation because they are unfolded, cleave BiP, or interact with IRE1