Research

Biochemistry/function of T7SS effector EsxA and impact on host barriers and inflammation.
In previous studies, we observed that the GBS T7SS contributes to cytotoxicity and the progression of meningitis, likely due to the pore-forming activity of key T7SS effector EsxA. Moving forward, research in the Spencer lab will investigate molecular mechanisms underlying EsxA pore-forming activity, damage to host barriers, as well as inflammatory response associated with neonatal bacteremia and meningitis.

Contribution of T7SS toxins to GBS mucosal colonization.
In recent work, we have characterized the first T7-secreted GBS LXG toxin and demonstrated its role in vaginal colonization and interbacterial competition. We also identified potential chaperones and immunity factors involved in toxin secretion and neutralization. However, the mechanisms governing GBS LXG toxin secretion and its function during mucosal colonization remain unclear. Future projects in the Spencer lab will investigate LXG toxin function in interbacterial competition and explore the impact of T7SS antagonism on the microbiota, mucosal barriers, and immunity in the colonizing niches of the vaginal tract and the neonatal intestine.