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Inflammation may cause preterm labor and fetal deaths

CLEVELANDInflammation from bacterial infections is linked to preterm births and deaths, according to researchers from Case Western Reserve Universitys School of Dental Medicine and the Case School of Medicine. They found if receptors responding to the presence of dead or living bacteria in the placentas of mice can be blocked, the number of preterm deaths will decline by nearly half.

Yiping Han along with Hongqi Lui from the Case Western Reserve dental school and Raymond Redline from the Case medical school report results from their investigation, TLR4 promotes F. nucleatum-induced fetal death in mice, in the Journal of Immunology.

New findings from the mouse study holds potential to develop ways to curb the emotional and economic toll on families that lose babies to preterm labor and fetal death, said Han, a member of from the department of periodontics.

Currently antibiotic treatments are not very effective at preventing preterm births that are triggered by a bacterial infection. Mice, as well as humans, have several toll-like receptors (TLR) that sense the surface components of living or dead bacteria. TLR2 and 4 are key receptors in recognizing bacterial surfaces. The investigators concentrated their study on these two receptors as a possible link in producing the inflammatory response that is believed to have brought about the fetal death in mice.

In a prior mouse study at Case Western Reserve, the investigators noted that inflammation closely paralleled localization of bacteria. In the present study, the researchers found that mice deficient in TLR4 lacked the necro-inflammatory response to bacteria and produced healthy pups. This discovery led Han and her colleagues to attempt to block the inflammatory process by using synthetic TLR4 antagonist that prevented the receptor from sensing the bacteria.

Fusobacterium nucleatum, a common oral pathogen also found in the amniotic fluid of preterm babies,
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Contact: Susan Griffith
susan.griffith@case.edu
216-368-1004
Case Western Reserve University
8-Aug-2007


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