Understanding the Role of Danger Associated Molecular Patterns in Fetal Membrane Weakening
Research Summary: During my first year as an INBRE Teaching Post-Doctoral Fellow I taught two undergraduate Biology courses within the Natural Science and Mathematics Department at Chaminade University of Honolulu. As a second year fellow my plan is to continue teaching undergraduate Biology courses and a lab during the upcoming academic school year. In addition to teaching, I conduct research under the mentorship and support of Dr. Claire Kendal-Wright at Chaminade.
Preterm birth occurs prior to 37 weeks of gestation and is the leading cause of infant death worldwide. According to the 2019 March of Dimes preterm birth report card, Hawaii currently has a C- rating, with a 10.3% preterm birth rate that has not improved within the last decade.
Inflammation initiated by infection is a known cause of preterm birth through the activation of toll like receptors (TLRs), however, some preterm births cases are idiopathic. Inflammation in the absence of infection, termed sterile inflammation, can be activated by danger associated molecular patterns (DAMPs), such as dsDNA. Therefore, one potential DAMP that could activate sterile inflammation through TLR9 and lead to fetal membrane weakening is cell free fetal DNA (cffDNA). Others in our field have data to support the importance of infection mediated fetal membrane weakening leading to PTB, however, little is known about sterile inflammation in this context. My research project objectives are 1) to understand the role of cffDNA in TLR9 activation in fetal membranes and 2.) develop a 3D model to understand the behavior of amnion cells from human fetal membranes upon cffDNA treatment. The completion of these objectives will strengthen our understanding of the mechanisms involved in inflammation mediated fetal membrane weakening leading to parturition.
