Skip to main content
. Author manuscript; available in PMC: 2009 Nov 30.
Published in final edited form as: J Immunol. 2009 Jun 26;183(2):1144–1154. doi: 10.4049/jimmunol.0900788

Figure 1. Dose dependent CpG ODN-mediated induction of fetal resorption and preterm birth in WT or IL-10−/− mice.

Figure 1

CpG or control ODN was injected i.p. in WT or IL-10−/− mice after visualization of a vaginal plug on gd0. (A) Fetal resorption in uterine horns from IL-10−/− or WT mice was assessed visually on gd9, mice were injected with CpG or control ODN on gd6. 25 µg of CpG ODN induced full resorption of uterine horns in IL-10−/− mice (n=37), whereas control ODN failed to elicit this pathology (n=20). WT mice did not respond to 25 µg CpG ODN, nor control ODN. (B) gd14 i.p. injection of 15 µg CpG ODN induced preterm birth of stillborn pups within 24–48 hours post injection in IL-10−/− mice (n=15). Control ODN-treated IL-10−/− mice did not experience preterm delivery (n=4). WT mice at this dose did not experience any preterm birth in the control ODN-condition (n=4) or CpG ODN-condition (n=4). (C) In WT mice a dose of 400 µg CpG ODN given i.p. on gd6 caused cranial-facial, and distal limb malformations, denoted by *, in 43% of pups born at term (n=12). Similarly, a dose of 300 µg CpG ODN in WT mice given i.p. on gd14 resulted in pups born at term with similar malformations (n=8). WT mice treated with control ODN at these doses did not display teratogenic effects.