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Contribution of Group B Streptococcal adhesin BspC to neonatal intestinal colonization and interactions with Candida albicans

Award Number: F31AI200351
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/16/2027
PERIOD OF PERFORMANCE END DATE: 01/15/2028

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Contribution of Group B Streptococcal adhesin BspC to neonatal intestinal colonization and interactions with Candida albicans - Project Summary Streptococcus agalactiae, or Group B Streptococcus (GBS) is the leading cause of neonatal meningitis worldwide. Though GBS benignly colonizes the intestinal and female reproductive tract in 30% of healthy adults, exposure to GBS can lead to invasive disease in neonates. Prophylactic intrapartum antibiotics have significantly reduced the incidence of early-onset disease, but late-onset disease, occurring 7 to 90 days post birth, currently has no preventative measures. In these cases, colonization of the neonatal gastrointestinal tract can lead to serious invasive disease with ongoing neurological sequalae in 50% of survivors. The mechanisms by which GBS colonizes the intestinal tract are not well defined, and we aim to better characterize this step in disease progression. Surface-anchored antigen I/II family adhesins are a widespread virulence factor among streptococcal species, serving to promote bacterial adhesion to host cells. In GBS, Group B streptococcal surface protein C (BspC) is particularly associated with hypervirulent meningitis-associated sequence type 17 (ST-17) strains and has been shown to promote GBS adherence to vaginal epithelial cells. We hypothesize that BspC contributes to GBS' ability to colonize the intestinal tract. Preliminary data reveals that an isogenic bspC mutant in the ST-17 strain COH1 displays significantly impaired adherence to both Caco-2 and primary human infant colonic epithelial cells compared to its wildtype counterpart. Recombinant BspC has been shown to interact with intermediate filament protein cytokeratin 19 (K19), and treatment of Caco-2 cells with a K19-specific antibody significantly reduced GBS adherence, indicating the importance of this interaction in BspC-mediated adherence. In a neonatal murine meningitis model, mice infected with bspC GBS survived significantly better than wildtype infected mice, along with displaying significantly reduced intestinal bacterial burden, supporting a role for BspC in colonization in vivo. Interestingly, BspC has been shown to contribute to GBS interactions with the fungus Candida albicans. C. albicans is an opportunistic fungal pathogen that colonizes the neonatal intestinal tract and is also responsible for significant invasive disease in premature neonates. Our experiments have shown that the presence of C. albicans enhances GBS adherence to intestinal epithelial cells. From these preliminary data, I hypothesize that BspC contributes to GBS persistence in the neonatal GI tract through both direct interaction with intestinal epithelial cells and indirectly through interaction with C. albicans, leading to the opportunity for progression to invasive disease. I will address these hypotheses with the following aims: Aim 1: Characterize the mechanisms by which BspC promotes GBS neonatal intestinal colonization; Aim 2: Assess the effect of Candida albicans on GBS intestinal colonization. The studies outlined in this proposal will increase our understanding of how bacterial virulence factors could serve as therapeutic targets to inhibit GBS intestinal colonization, and consequentially limit neonatal invasive GBS disease.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $38,597 )
2026	2026	THE REGENTS OF THE UNIVERSITY OF COLORADO	13001 E 17TH PL STE F428	AURORA	CO	80045	ADAMS	USA	Allergy and Infectious Diseases Research	000	1	7/16/2026	NEW	$38,597
														Subtotal = $38,597

Grand Total All Awards = $38,597

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Contribution of Group B Streptococcal adhesin BspC to neonatal intestinal colonization and interactions with Candida albicans

Award Number: F31AI200351

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/16/2027

PERIOD OF PERFORMANCE END DATE: 01/15/2028

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