Reply to Noori et al., “A Complex Scenario of Nonsteroidal Anti-inflammatory Drugs Induced Prostaglandin E2 Production and Gut Microbiota Alteration in Clostridium difficile-Infected Mice”

摘要

We thank Noori and colleagues for their interest in our recent work and appreciate their interpretation of the data from our study in the context of other existing data ( 1 ). They underscore an interesting finding in our study: colon levels of the lipid mediator prostaglandin E2 (PGE _(2)) paradoxically increased during Clostridioides difficile infection (CDI) following a brief exposure to the nonsteroidal anti-inflammatory drug (NSAID) indomethacin, which is known to inhibit PG synthesis ( 2 ). This increase in tissue PGE _(2) was associated with marked tissue inflammation, upregulation of the inducible PGE synthase enzyme encoded by the PTGES gene, and suppression of the PGE _(2)-inactivating enzyme 15-PG dehydrogenase (15-PGDH), encoded by the HPGD gene ( 2 ).