Presentation Type
Poster Presentation
Abstract
Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease primarily affecting premature infants. Toll-like receptor 4 (TLR4)-mediated epithelial damage allows microbial translocation, triggering inflammation that can lead to sepsis and death. The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, and AhR ligands have been shown to prevent NEC in a mouse model. Indole, an AhR ligand, has been reported to extend the healthspan of C. elegans, and we have shown previously it mitigates poor outcomes in wild-type worms infected with Cronobacter sakazakii (Cs), a bacterial pathogen linked to NEC. We hypothesized that C. elegans must express ahr-1, the ortholog of human AHR, for indole to confer protection against Cs infection. To test this, we used ZG24 C. elegans, an ahr-1 knockout strain, and performed a larval stage 4 (L4) killing assay. Worms were infected with Cs on day 0 and treated with either indole or methanol (vehicle control) on days 1 and 4. We monitored motility over seven days and conducted a heat stress assay on day 7 to assess health. Our results showed no difference in health outcomes between Cs-infected worms treated with indole versus methanol, indicating that indole-mediated protection requires AhR activity. These findings highlight AhR ligands as potential therapeutic candidates for NEC and support further investigation into their protective mechanisms.
Faculty Mentor
Dr. Kyle Brawner
Recommended Citation
Durrough, Cayden, "Indole improves outcomes of Cronobacter sakazakii infection in C. elegans through ahr-1" (2025). Student Scholar Symposium. 144.
https://digitalcollections.lipscomb.edu/student_scholars_symposium/2025/Full_schedule/144
Included in
Indole improves outcomes of Cronobacter sakazakii infection in C. elegans through ahr-1
Necrotizing enterocolitis (NEC) is a severe gastrointestinal disease primarily affecting premature infants. Toll-like receptor 4 (TLR4)-mediated epithelial damage allows microbial translocation, triggering inflammation that can lead to sepsis and death. The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, and AhR ligands have been shown to prevent NEC in a mouse model. Indole, an AhR ligand, has been reported to extend the healthspan of C. elegans, and we have shown previously it mitigates poor outcomes in wild-type worms infected with Cronobacter sakazakii (Cs), a bacterial pathogen linked to NEC. We hypothesized that C. elegans must express ahr-1, the ortholog of human AHR, for indole to confer protection against Cs infection. To test this, we used ZG24 C. elegans, an ahr-1 knockout strain, and performed a larval stage 4 (L4) killing assay. Worms were infected with Cs on day 0 and treated with either indole or methanol (vehicle control) on days 1 and 4. We monitored motility over seven days and conducted a heat stress assay on day 7 to assess health. Our results showed no difference in health outcomes between Cs-infected worms treated with indole versus methanol, indicating that indole-mediated protection requires AhR activity. These findings highlight AhR ligands as potential therapeutic candidates for NEC and support further investigation into their protective mechanisms.