Elevated prostaglandin E₂ post-bone marrow transplant mediates interleukin-1β-related lung injury.

ABSTRACT: Hematopoietic stem cell transplant (HSCT) treats or cures a variety of hematological and inherited disorders. Unfortunately, patients who undergo HSCT are susceptible to infections by a wide array of opportunistic pathogens. Pseudomonas aeruginosa bacteria can have life-threatening effects in HSCT patients by causing lung pathology that has been linked to high levels of the potent pro-inflammatory cytokine, interleukin-1β (IL-1β). Using a murine bone marrow transplant (BMT) model, we show that overexpression of prostaglandin E₂ (PGE₂) post-BMT signals via EP2 or EP4 to induce cyclic adenosine monophosphate (cAMP), which activates protein kinase A or the exchange protein activated by cAMP (Epac) to induce cAMP response element binding-dependent transcription of IL-1β l

SUBMITTER: Martinez-Colon GJ 

PROVIDER: S-EPMC5720939 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature