Presenting Author: Jordan K Vance
, PhD Candidate at West Virginia Univ. Sch. of Med.
Abstract:
Neonates are more susceptible to infection due to the unique immune profile during infancy. We have shown that interleukin (IL)‑27, an immune suppressive cytokine, is elevated in both newborn mice and humans. Using a murine model of neonatal bacterial sepsis, we have shown that IL-27 levels further increase and negatively affect clearance and survival of infection. A variety of cell types are capable of IL-27 production, however the primary tissues and specific cell populations supplying IL-27 during sepsis have not been described. This work profiled IL‑27‑producers from tissues in which we have shown increased IL‑27 transcripts using our established model of gram-negative neonatal sepsis in IL‑27p28eGFP reporter mice. The abundance of IL‑27‑producing myeloid cells significantly increased in the livers of Escherichia coli-infected mice. Many IL‑27‑producers were F4/80+CD11b+ during homeostasis and infection, however septic hepatocytes exhibited changes in expression of F4/80, CD11c, and MHC II accompanied by an overall increase of CD11b. Our results show macrophage subpopulations responsible for IL-27 with potentially unique functions in the disease state. These data suggest important changes in IL‑27‑producers during neonatal bacterial sepsis. This work is essential in understanding IL‑27‑producers and the effect on bacterial clearance during neonatal bacterial sepsis, which could support IL‑27 as a target for therapeutic approaches to treat neonatal bacterial sepsis.
The Face of IL-27 Production During Murine Neonatal Bacterial Sepsis
Category
Poster and Podium (Block Symposium)
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Date: May 6 Presentation Time: 11:30 AM to 12:45 PM Room: Exhibit Hall F1