Abstract
Quorum sensing (QS) allows bacteria to communicate with one another by means of QS signaling molecules and control certain behaviors in a group-based manner, including pathogenicity and biofilm formation. Bacterial gut microflora may play a role in inflammatory bowel disease pathogenesis, and antibiotics are one of the available therapeutic options for Crohn's disease. In the present study, we employed genetically engineered bioluminescent bacterial whole-cell sensing systems as a tool to evaluate the ability of antibiotics commonly employed in the treatment of chronic inflammatory conditions to interfere with QS. We investigated the effect of ciprofloxacin, metronidazole, and tinidazole on quorum sensing. Several concentrations of individual antibiotics were allowed to interact with two different types of bacterial sensing cells, in both the presence and absence of a fixed concentration of N-acylhomoserine lactone (AHL) QS molecules. The antibiotic effect was then determined by monitoring the biosensor's bioluminescence response. Ciprofloxacin, metronidazole, and tinidazole exhibited a dose-dependent augmentation in the response of both bacterial sensing systems, thus showing an AHL-like effect. Additionally, such an augmentation was observed, in both the presence and absence of AHL. The data obtained indicate that ciprofloxacin, metronidazole, and tinidazole may interfere with bacterial communication systems. The results suggest that these antibiotics, at the concentrations tested, may themselves act as bacterial signaling molecules. The beneficial effect of these antibiotics in the treatment of intestinal inflammation may be due, at least in part, to their effect on QS-related bacterial behavior in the gut.
| Original language | English |
|---|---|
| Pages (from-to) | 3227-3236 |
| Number of pages | 10 |
| Journal | Analytical and Bioanalytical Chemistry |
| Volume | 402 |
| Issue number | 10 |
| DOIs | |
| State | Published - Apr 2012 |
Funding
Acknowledgments This work was partly supported by the National Science Foundation (Grant CHE-0416553), the Children’s Miracle Network, and the Broad Foundation, Broad Medical Research Program (BMRP), Grant IBD-0198R. S.D. is grateful for support from the Lucille P. Markey Chair in Biochemistry and Molecular Biology of the Miller School of Medicine of the University of Miami, as well as from a Gill Eminent Professorship from the University of Kentucky. A. K.S. acknowledges support from a Gill Fellowship and a Research Challenge Trust Fund Fellowship from the University of Kentucky. We also thank Prof. Paul Williams (University of Nottingham, Nottingham, UK) for providing plasmids pSB406 and pSB1075.
| Funders | Funder number |
|---|---|
| Children’s Miracle Network | |
| University of Kentucky | |
| Miami Clinical and Translational Science Institute, University of Miami | |
| Eli and Edythe Broad Foundation | |
| National Science Foundation Arctic Social Science Program | CHE-0416553 |
| Broad Medical Research Program | IBD-0198R |
Keywords
- Antibiotics
- Bacterial whole-cell biosensing systems
- Bioluminescence
- Inflammatory bowel disease
- Quorum sensing
ASJC Scopus subject areas
- Analytical Chemistry
- Biochemistry