Abstract
Elevated temperatures during pregnancy can be detrimental for offspring survivability and can lead to developmental problems. To promote foetal health, mothers lose the ability to mount a fever in late pregnancy.
The lack of fever response during pregnancy has been described in rats, guinea pigs, and ewes. To understand the mechanism behind this adaptation, we first aimed to establish this model in mice. We used radio telemetry to monitor core body temperature in both non-pregnant and late pregnant wild type C57BL/6 mice. To induce a fever, mice were injected with either the bacterial mimetic, lipopolysaccharide (LPS, 50 g/kg s.c.) or the viral mimetic polyinosinic:polycytidylic acid (poly I:C, 80 mg/kg s.c.). In non-pregnant mice, LPS (n=9, repeated measures two-way ANOVA, P = 0.0017) and poly I:C (n=6, two-way ANOVA, P = 0.0282) injections induced a 1-2 C fever that lasted approximately 10 hours compared to the saline injected mice. However, in late pregnant (day 18 of pregnancy) mice, neither the LPS (n=9, two-way ANOVA, P = 0.1749) or the poly I:C (n=6, two-way ANOVA, P = 0.0914) caused a fever. We also monitored other sickness behaviours such as activity patterns and food intake. Compared to saline injected animals, we observed that the LPS and poly I:C injected animals had diminished activity and reduced food intake, both in the non-pregnant and the late pregnant mice.
Here we have established that during late pregnancy, mice show a diminished fever response following both a bacterial and a viral mimetic injection. However, both the LPS and the poly I:C-injected pregnant mice did develop other sickness symptoms suggesting that the thermal response to infection is suppressed in late pregnancy but not the anorexia and the lethargy. This research provides novel insights into the regulation of fever during pregnancy and establishes a model for studying this maternal adaptation in mice.