Evidence linking bacterial vaginosis (BV) to chorioamnionitis and spontaneous preterm birth is mounting. Successful treatment of BV could reduce the rate of late miscarriage and preterm birth. Mucinase and sialidase activity have been implicated in the pathogenesis of BV. This study extends the work of previous studies to investigate sialidase, other known mucin degrading enzymes and overall mucin degrading activity in samples of vaginal fluid from women with and without BV. Samples from 31 women were diagnosed for BV, and tested for enzyme activity using established assays. Activity was recorded in all samples. Significant increases in activity were detected in BV samples for sialidase using a mucin (BSM P<0.005) and serum type glycoprotein (AGP P<0.005) substrates, beta-galactosidase (P<0.001), and beta-N-acetylhexosaminidase (P<0.01). No significant increases in BV patients were detected in O-glycanase, proteinase, arylesterase, sulphatase or whole mucinase activities. These results support the hypothesis that certain BV-associated enzymes may detrimentally affect the mucosal barrier, permitting bacteria access to the uterus.

Interleukin-3 (IL-3), which can be derived from T cells and other sources, is well documented at promoting the in vitro differentiation and proliferation of murine hematopoietic progenitors, yielding multipotential blast cells, mast cells, and mature cells of the myeloid and erythroid lineages. Although IL-3-deficient (knockout [KO]) mice display intact steady-state hematopoiesis, administration of IL-3 to mice and humans can promote hematopoiesis and influence the effector functions of mature hematopoietic cells in vivo. Because of these biological activities of IL-3, the contribution of IL-3 to resistance to blood-stage malaria was investigated by infecting KO mice intraperitoneally with Plasmodium berghei-infected RBCs. We found that KO mice were more susceptible to infection than wild-type (WT) mice, as evidenced by markedly higher peak parasitemia. P. berghei-infected KO mice also had significantly greater anemia and splenomegaly compared to similarly infected WT mice. Our results indicate that IL-3 contributes to resistance to P. berghei infection.