Jamisha Francis

Group B streptococcal (GBS) or Streptococcus agalactiae infections are one of the top five leading causes of neonatal mortality, causing chorioamnionitis, fetal infection, neonatal sepsis and preterm birth. GBS colonizes the urogenital and/or the gastro-intestinal tract of about 40-50% of healthy women in the United States. Innate immune cells like neutrophils respond to GBS and deposit antimicrobial molecules like S100A-family proteins. S100A12 or Calgranulin C is a calcium binding proinflammatory protein that is secreted by granulocytes. Under conditions of low metal availability, S100A12 inhibits GBS growth via zinc chelation, a result that was reversed by the addition of exogenous zinc. In conditions of high zinc availability, S100A12 mitigates zinc stress in GBS and promotes biofilm formation on abiotic and biotic surfaces. Conversely, the addition of zinc represses bacterial biofilm formation on polystyrene, gestational membranes and the instrumented fetal membrane on a chip (IFMOC). GBS also mitigates zinc stress via deployment of the CadD efflux determinant, which aids in zinc detoxification. Our proposed Aims will seek to determine the role that cadD plays in promoting biofilm formation on gestational tissues, IFMOC, and in vivo under differing conditions of dietary zinc intake. These aims fit within the mission of the training grant and will promote investigation at the interface of chemistry and biology.

Mentor: Jennifer Angeline Gaddy, Ph.D.