RT are former employees of Compass Therapeutics and are partners in the LLC. UE, SQH, and WG are now employees of Akrevia Therapeutics. CC is now an employee of CRISPR Therapeutics. SO is now an employee of Bluebird Bio. RT and JL are now employees of TCR2 Therapeutics. PB is now an employee of Sanofi. MO is now an employee of Bristol-Myers Squibb. WFC is now an employee of Astellas Pharmaceuticals. ACA is a member of the scientific advisory board for Tizona Therapeutics, Compass Therapeutics, and Zumutor Biologics and is a paid consultant for Aximmune. ACA, CL, and CW received research funding from Compass Therapeutics. PB, MS, JL, RT, CLL, and UE are inventors on the following issued U.S. patents held by applicant Compass Therapeutics: patent nos. 10,279,038B2; 10,279,039B2; and 10,279,040B1; these patents cover pharmaceutical compositions comprising CTX-471 and methods of using CTX-471 for treating cancer or inducing antitumor immune response in cancer patients.

During pregnancy, GBS ascension into the uterus can cause fetal infection or preterm birth. In addition, GBS exposure during labor creates a risk of serious disease in the vulnerable newborn and mother postpartum.

UTI is one of the most common causes of outpatient antibiotic use, and rising antibiotic resistance threatens the ability to control UTI unless alternative treatments are developed. Bacteriophage (phage) therapy is gaining renewed interest; however, much like with antibiotics, bacteria can readily become resistant to phages.

Group B Streptococcus (GBS) colonizes the vaginal mucosa of a significant percentage of healthy women and is a leading cause of neonatal bacterial infections. Currently, pregnant women are screened in the last month of pregnancy and GBS-positive women are given antibiotics during parturition to prevent bacterial transmission to the neonate. Recently, human milk oligosaccharides (HMOs) isolated from breastmilk were found to inhibit GBS growth and biofilm formation in vitro, and women that make certain HMOs are less likely to be vaginally colonized with GBS. Using in vitro human vaginal epithelial cells and a murine vaginal colonization model, we tested the impact of HMO treatment on GBS burdens and the composition of the endogenous microbiota by 16S rRNA amplicon sequencing. HMO treatment reduced GBS vaginal burdens in vivo with minimal alterations to the vaginal microbiota. HMOs displayed potent inhibitory activity against GBS in vitro, but HMO pretreatment did not alter adherence of GBS or the probiotic Lactobacillus rhamnosus to human vaginal epithelial cells. Additionally, disruption of a putative GBS glycosyltransferase (Δsan_0913) rendered the bacterium largely resistant to HMO inhibition in vitro and in vivo but did not compromise its adherence, colonization, or biofilm formation in the absence of HMOs. We conclude that HMOs are a promising therapeutic bioactive to limit GBS vaginal colonization with minimal impacts on the vaginal microenvironment.