Inflammation during pregnancy can disturb maternal tolerance of the fetus. In mice, maternal high-fat diet (HFD) induces inflammation without pregnancy complications. I hypothesised that an additional inflammatory insult would exacerbate the immune response, leading to serious complications. To test this, I developed a HFD/LPS model, where female mice were fed a high-fat or low-fat diet prior to mating, and then treated with either bacterial lipopolysaccharide (LPS), an inflammatory stimulant, or a control. Diet, LPS or a diet-LPS interaction had no effect on fetal and placental parameters or maternal levels of TNF-α, an inflammatory marker (p>0.05). Furthermore, fetal and placental parameters did not differ between HFD mice that were prone or resistant to weight-gain. While diet or a diet-LPS interaction did not affect pregnancy, LPS treatment alone caused complete fetal loss in some mice (p
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Thesis advisor: Christians, Julian
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