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. 2018 Oct 31;9:2447. doi: 10.3389/fmicb.2018.02447

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Copyright © 2018 Sheppe, Kummari, Walker, Richards, Hui, Lee, Mangum, Borazjani, Ross and Edelmann.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Model of the effects of PGE2 secretion during infection with Gram-negative bacteria S. Typhimurium and Y. enterocolitica. Bacterial pathogens can stimulate the production of PGE2 from AA by activating COX-2 via TLR-LPS signaling or through other virulence factors such as Salmonella SpiC or Yersinia YopM. PGE2 is secreted and acts locally on EP2/EP4 receptors to repress M2 macrophage gene transcription by SOCS3. PGE2 increases IL-1β and IL-12βp40 transcription. The immature IL-1β is converted to mature IL-1β by activated caspase-1 during inflammasome activation and secreted into the environment. Inflammasomes can be stimulated or inhibited by specific bacterial components and virulence factors such as bacterial flagellin, or by YopM/SopB in Y. enterocolitica and S. Typhimurium, respectively.