Related Experiment Videos
Bacterial protease-induced reduction of chorioamniotic membrane strength and elasticity
Abstract:
We demonstrated that in vitro exposure to bacterial collagenase and collagenase-producing microorganisms significantly reduces measures of strength (bursting load), elasticity, and work to rupture of human amniochorion in a dose-dependent fashion. An attenuated noncollagenase-producing stain did not alter these measures. These findings support previous suggestions that infection within the lower uterine segment adjacent to the cervix may mediate some instances of premature rupture of membranes.
Insights
Bacterial collagenase and collagen-producing microbes weaken human amniochorion tissues. This supports infection as a cause of premature rupture of membranes.
Area of Science:
- Obstetrics and Gynecology
- Microbiology
- Biomedical Engineering
Background:
- Premature rupture of membranes (PROM) is a leading cause of preterm birth.
- The role of infection, particularly bacterial enzymes, in PROM is not fully understood.
Purpose of the Study:
- To investigate the impact of bacterial collagenase on the biomechanical properties of human amniochorion.
- To determine if collagenase-producing microorganisms can degrade amniochorion tissue.
Main Methods:
- In vitro exposure of human amniochorion samples to bacterial collagenase and collagenase-producing bacteria.
- Measurement of biomechanical properties including bursting load, elasticity, and work to rupture.
- Comparison with samples exposed to an attenuated noncollagenase-producing strain.
Main Results:
- Exposure to bacterial collagenase and collagenase-producing microorganisms significantly reduced amniochorion strength, elasticity, and work to rupture.
- These effects were dose-dependent.
- An attenuated noncollagenase-producing strain did not affect tissue properties.
Conclusions:
- Bacterial collagenase activity is detrimental to the biomechanical integrity of the human amniochorion.
- Infection in the lower uterine segment may contribute to premature rupture of membranes by degrading protective tissues.