Toll Like Receptors and Inflammation During Pregnancy.

Abstract

Infection in infants continues to be the major global cause of morbidity and mortality despite international childhood vaccination programs. The cost of infants' hospitalization due to infections is estimated at 690 million dollars annually in the US alone. While most vaccines do induce protection in some children, their efficacy and response is not the same in all infants. The establishment of a functional immune system in all mammals requires a sequential series of carefully tuned and coordinated developmental events beginning early in embryonic/fetal life and continuing through the early postnatal period. The increasing repertoire of health conditions being linked to in-utero exposures has recently expanded leading to the concept that maternal signals lead to fetal programming and subsequent effects on the well being of the adult. Little is known about the potential in-utero programming effects on immune function. Recent studies from our laboratory and others suggest that maternal inflammation or infection during pregnancy not only increases the likelihood of adverse pregnancy outcome, but could also contribute to abnormal development of the fetal immune system. Here, we will discuss new data associated with the inflammatory process initiated as a response of the placenta to viral infection which will have a significant effect on fetal development. We propose that in normal conditions the female reproductive tract prevents immune responses to bacterial products, which are a natural component of the tract, in order to avoid a chronic state of inflammation. Viral infection may this state of homeostasis. If the infection occurs during pregnancy, the outcome of the pregnancy may be jeopardized. Our objective is to elaborate on the mechanisms mediating the changes associated with viral and bacterial infection during pregnancy.