PROBLEM: Preterm, premature rupture of membranes (PPROM) is a dire pregnancy 
outcome that is frequently associated with infection by the genital mycoplasmas, 
Mycoplasma hominis, Ureaplasma parvum, and U. urealyticum. One potential 
mechanism by which these microorganisms may cause PPROM is by increasing the 
concentration of matrix metalloproteinases (MMPs) in the membranes and amniotic 
fluid. We tested this hypothesis in a well-defined model system of genital 
infection with M. pulmonis, a natural reproductive pathogen of rats.
METHOD OF STUDY: Timed-pregnant, specific pathogen-free, Sprague-Dawley rats 
were infected with 10(7) CFU M. pulmonis at gestation day (gd) 14. Controls 
received an equivalent volume (100 microL) of sterile medium. At gd 18, rats 
were euthanized, and membranes and amniotic fluids were harvested and stored at 
-70 degrees C until analysis. Proteinase activity of amniotic fluid and 
membranes was resolved on discontinuous 7.5% sodium dodecyl 
sulfate-polyacrylamide gel electrophoresis gelatin zymography gels. Band 
intensity was determined using a digital gel documentation system and the 
manufacturer's software (Kodak).
RESULTS: Gelatinolytic activity associated with a band similar in molecular 
weight to ProMMP-9 (92 kDa, the inactive precursor of MMP-9) was significantly 
increased in amniotic fluids and membranes harvested from M. pulmonis-treated 
pups at gd 18 when compared with tissues harvested from control pups. Both 
ProMMP-9 and ProMMP-2 (72 kDa, the inactive precursor of MMP-2) were increased 
in infected animals at gd 21.
CONCLUSION: Our study suggests that the genital mycoplasmas can increase MMP-9 
production in vivo.