# Contact-dependent suppression of Clostridioides difficile sporulation by enterococci

> **NIH NIH R03** · STATE UNIVERSITY OF NY,BINGHAMTON · 2024 · $78,909

## Abstract

Sporulation by Clostridioides difficile occurs naturally in the gut among other bacteria such as enterococci,
which are present in all animals. The long-term goal of this laboratory is to define the mechanistic basis of
bacteria-bacteria and host interactions that modulate virulence of C. difficile. The overall objective of this
proposal is to discover genetic factors involved in a potential proximity-dependent inhibition of C. difficile
sporulation by enterococci. The central hypothesis is that enterococci suppress C. difficile sporulation via
interactions at the cell surface. The rationale for this project is that determination of mechanisms of
interaction between the two species will allow the development of treatments that limit the potential for C.
difficile infection. Based on preliminary data, our overall working hypothesis for this proposal is: E. faecalis
inhibits sporulation via its surface proteins when in cell-cell contact with C. difficile. To attain the overall
objectives these two specific aims will be pursued: Aim 1) Identify genes in Enterococcus faecalis OG1RF
that are involved in proximity-dependent inhibition of C. difficile sporulation. In these experiments, we will
use an arrayed library of transposon insertion mutants to screen for genes in E. faecalis involved in
suppression of sporulation. Aim 2) Define the transcriptional network of enterococci-mediated sporulation
inhibition. We will develop a well calibrated transwell co-culture assay and will perform transcriptional
profiling during induction of sporulation to determine genes involved in this phenomenon. The research
proposed is innovative in the applicant’s opinion because it focuses specifically on interactions between
two gastrointestinal pathogens and how cell contact with non-kin bacteria regulates a cell fate decision.
The proposed research is significant because it will provide a context for understanding how enterococci,
which commonly expand in antibiotics-treated patients, affect the balance between spore formation and
vegetative toxin-producing C. difficile.

## Key facts

- **NIH application ID:** 10988567
- **Project number:** 1R03AI180614-01A1
- **Recipient organization:** STATE UNIVERSITY OF NY,BINGHAMTON
- **Principal Investigator:** Peter T McKenney
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $78,909
- **Award type:** 1
- **Project period:** 2024-05-23 → 2026-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10988567

## Citation

> US National Institutes of Health, RePORTER application 10988567, Contact-dependent suppression of Clostridioides difficile sporulation by enterococci (1R03AI180614-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10988567. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*