Bacterial load and inflammation in fetal tissues is not dependent on IL-17a or IL-22 in 10-14 day pregnant mice infected with Listeria monocytogenes.

In this study, we first assessed the effect of intragastric infection of pregnant mice with Listeria monocytogenes on relative expression of select genes associated with T cell subsets. Relative gene expression was moderately increased in placental tissues for IFNγ, IL-4, IL-17a, IL-22, CD3, and FoxP3. To assess the roles of IL-17a and IL-22 in resistance to listeriosis during pregnancy, we compared the severity of maternal and fetal infection in IL-17a((-/-)), IL-22((-/-)), and IL-17a((-/-))/IL-22((-/-)) mice with that of wild type C57BL/6 mice. Intragastric infection with modest numbers of bacterial cells (10(5) CFU) caused reproducible maternal and fetal infection in all four mouse strains. We recovered greater numbers of CFU from the bloodstream of pregnant IL-22((-/-)) mice than pregnant wild type mice. Otherwise we found no significant difference in bacterial load in maternal or fetal tissues (spleen, liver, fetoplacental units) from pregnant IL-17a((-/-)), IL-22((-/-)), or IL-17a((-/-))/IL-22((-/-)) or wild type mice. Nor did we observe histopathologic differences in severity of inflammation in maternal or fetal tissues from the various groups of mice. Although IL-17a and IL-22 are up-regulated in placental tissue, our study suggests that antibacterial resistance and the host inflammatory response are not dependent on IL-17a or IL-22 during infection of mice with L. monocytogenes at 10-14 days of gestation.