Immunological and pathological changes after maternal exposure with Listeria monocytogenes in pregnant guinea pigs

Abstract

Listeriosis has the highest case fatality rate of foodborne illnesses in the United States, approximately 30%. One-third of the 2500 cases involve the fetus or neonate. The mechanisms of fetal infection and death are largely unknown. The objectives of this study were to use pregnant guinea pigs 1) to determine effects of exposure to L. monocytogenes on apoptosis in the placenta, 2) to characterize maternal serum cytokine levels after exposure to L. monocytogenes, 3) to determine infection-related changes in placental cytokine expression, 4) to determine the immunoreactivity of a human anti E-cadherin antibody to intestinal and placental tissue. Oral inoculation of pregnant guinea pigs resulted in an increase in the number of placentas undergoing apoptosis at > 10 CFUs L. monocytogenes at 21 days post-treatment. Maternal serum TNF-alpha. levels were significantly decreased 21 days post treatment at > 10 CFUs L. monocytogenes. After maternal treatment with 10 CFUs L. monocytogenes, placental inflammatory cytokine expression was altered as early as six days post-treatment. At 10 CFUs L. monocytogenes, an increasing trend of placental apoptosis was seen as infection proceeded. Guinea pig and rhesus monkey intestinal tissue was immunoreactive to a human anti E-cadherin antibody. In conclusion, the placental cytokine expression and apoptosis is affected after maternal infection with L. monocytogenes. TNF-alpha. concentrations in maternal serum were significantly decreased after oral exposure to L. monocytogenes. A better understanding of mechanisms behind Listeria-induced stillbirths will allow for the development of biomarkers for infection and treatment capabilities.