Olivia Walsh
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Interests
Olivia Walsh has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Carly Hennessey
University of California Davis, United States
1 shared publication - Colin Reardon
Department of Anatomy, Physiology, and Cell Biology, UC Davis School of Veterinary Medicine, UC Davis, Davis, CA, USA
1 shared publication - Gonzalo Rabasa
University of California Davis, United States
1 shared publication - Ingrid Brust-Mascher
Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA
1 shared publication - Jessica A. Sladek
University of California Davis, United States
1 shared publication - Mackenzie K. Honeycutt
Veterans Affairs Puget Sound Health Care System, USA
1 shared publication
Latest Publications
- Open Access
Neonatal enteropathogenic Escherichia coli infection disrupts microbiota-gut-brain axis signaling
Background: Diarrheal diseases are a leading cause of death in children under age five worldwide. Repeated early life exposures to diarrheal pathogens can result in co-morbidities including stunted growth and cognitive deficits suggesting an impairment in the microbiota-gut-brain (MGB) axis. Methods: Neonatal C57BL/6 mice were infected with EPEC (strain e2348/69; ΔescV [T3SS mutant]), or vehicle (LB broth) via orogastric gavage (10 5 CFU) at post-natal day (P7). Behavior (novel object recognition [NOR] task, light/dark [L/D] box, and open field test [OFT]), intestinal physiology (Ussing chambers), and the microbiota (16S Illumina sequencing) were assessed in adulthood (6-8 weeks). Results: Neonatal infection of mice with EPEC impaired recognition memory (NOR task), coupled with increased neurogenesis (Ki67 and doublecortin immunostaining) and neuroinflammation (increased microglia activation [Iba1]) in adulthood. Intestinal pathophysiology was characterized by increased secretory state (short circuit current; Isc) and permeability (conductance; FITC-dextran flux) in the ileum and colon of neonatally EPEC-infected mice, along with increased expression of pro-inflammatory cytokines ( Tnfα, Il12, Il6 ) and pattern recognition receptors ( Nlr, Tlr ). Finally, neonatal EPEC infection caused significant dysbiosis of the gut microbiota, including decreased Firmicutes, in adulthood. Conclusions: Together these findings demonstrate that infection in early life can significantly impair the MGB axis in adulthood.
Open AccessNeonatal enteropathogenic Escherichia coli infection disrupts microbiota-gut-brain axis signaling
Background: Diarrheal diseases are a leading cause of death in children under age five worldwide. Repeated early life exposures to diarrheal pathogens can result in co-morbidities including stunted growth and cognitive deficits suggesting an impairment in the microbiota-gut-brain (MGB) axis. Methods: Neonatal C57BL/6 mice were infected with EPEC (strain e2348/69; ΔescV [T3SS mutant]), or vehicle (LB broth) via orogastric gavage (10 5 CFU) at post-natal day (P7). Behavior (novel object recognition [NOR] task, light/dark [L/D] box, and open field test [OFT]), intestinal physiology (Ussing chambers), and the microbiota (16S Illumina sequencing) were assessed in adulthood (6-8 weeks). Results: Neonatal infection of mice with EPEC impaired recognition memory (NOR task), coupled with increased neurogenesis (Ki67 and doublecortin immunostaining) and neuroinflammation (increased microglia activation [Iba1]) in adulthood. Intestinal pathophysiology was characterized by increased secretory state (short circuit current; Isc) and permeability (conductance; FITC-dextran flux) in the ileum and colon of neonatally EPEC-infected mice, along with increased expression of pro-inflammatory cytokines ( Tnfα, Il12, Il6 ) and pattern recognition receptors ( Nlr, Tlr ). Finally, neonatal EPEC infection caused significant dysbiosis of the gut microbiota, including decreased Firmicutes, in adulthood. Conclusions: Together these findings demonstrate that infection in early life can significantly impair the MGB axis in adulthood.