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. 2002 Nov 13;26(1):17–30. doi: 10.1016/0165-0378(93)00863-O

Evaluation of the role of exogenous pathogens on the incidence of embryo loss during early pregnancy in mice

MG Baines a,, KA Billingsley a, AR De Fougerolles a, AJ Duclos a, HJ Olney a, DK Pomerantz b, RL Gendron c
PMCID: PMC7127243  PMID: 8040834

Abstract

The mating of CBA/j♀ mice (H2k) by DBA/2j♂ mice (H2d) typically results in an elevated incidence of spontaneous embryo loss thus providing an ideal genetically controlled laboratory model for the study of the factors causing early embryo loss during pregnancy. There is now considerable data on the cells and factors involved in fetal resorption but little is known about the events which activate this process. While the activation of the maternal response to the fetal implant could have endogenous or genetic origins, a role for exogenous factors including microbial pathogens could also be involved. In order to investigate these possibilities, the reproductive success of CBA/j♀ × DBA/2j♂ matings in a conventional animal care facility were compared with matings in a specific pathogen free (SPF) animal facility. All animals housed under these conditions were routinely screened by immunoassay and culture, for the presence of a number of viral and bacterial pathogens of mice. The incidence of spontaneous embryo loss in specific pathogen free CBA female mice mated by DBA and other male strains was found to be virtually identical to that of CBA female mice infected with multiple viral pathogens and housed under otherwise identical conditions (non-SPF). However, the numbers of implantation per pregnancy was significantly greater in an SPF facility. Therefore, exposure of mating mice to exogenous viral and bacterial pathogens did not appear to alter the overall incidence of spontaneous embryo resorption. It was concluded that the immunomodulatory effects of infection by common murine pathogens neither augmented nor reduced post-implantation embryo losses.

Keywords: Pregnant, Spontaneous abortion, Resorption, Pathogens, Infection

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