Meanwhile, in related investigations, researchers discovered that in nearly 80 percent of the cases of preterm labor, bacteria are present in the amniotic fluid. Plessinger's lab has been focusing on the association between the infectious organisms and the amniotic fibroblasts, zeroing in on E. coli as a potential culprit. (Many premature babies test positive for E. coli.)
Plessinger hypothesizes that when the mother's body tries to fight off the offending bacteria, the TLRs activate and cause inflammation. The inflammatory cells brought in to kill off the infectious microbes may pump naturally occurring hypochlorous acids and enzymes from the body into the fetal membranes, causing them to break apart and rupture.
Plessinger and colleagues Melanie O'Bara and Dongdong Guo, discovered the existence of the toll-like receptors and their role in fueling an inflammatory response after they had isolated amniotic cells from women who experienced normal, full-term delivery and cells from women who went into early labor.
"The big question is: What is it about the inflammatory process that impacts the fetal membranes and starts the entire chain of events that leads to early labor?" Plessinger said. "We are on a path to discovering that answer, and we hope it will lead us to the development of a new class of drugs that can shut down the process of premature delivery."