Prostaglandin E2 Regulation of Macrophage Innate Immunity.

Kimmel DW, Rogers LM, Aronoff DM, Cliffel DE
Chem Res Toxicol. 2016 29 (1): 19-25

PMID: 26656203 · DOI:10.1021/acs.chemrestox.5b00322

Globally, maternal and fetal health is greatly impacted by extraplacental inflammation. Group B Streptococcus (GBS), a leading cause of chorioamnionitis, is thought to take advantage of the uterine environment during pregnancy in order to cause inflammation and infection. In this study, we demonstrate the metabolic changes of murine macrophages caused by GBS exposure. GBS alone prompted a delayed increase in lactate production, highlighting its ability to redirect macrophage metabolism from aerobic to anaerobic respiration. This production of lactate is thought to aid in the development and propagation of GBS throughout the surrounding tissue. Additionally, this study shows that PGE2 priming was able to exacerbate lactate production, shown by the rapid and substantial lactate increases seen upon GBS exposure. These data provide a novel model to study the role of GBS exposure to macrophages with and without PGE2 priming.

MeSH Terms (9)

Animals Cell Line Dinoprostone Immunity, Innate Lactic Acid Lipopolysaccharides Macrophages Mice Streptococcus

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