The Role of Vitamin D Deficiency on Innate Lymphoid Cell Activity and the Severity of Citrobacter rodentium Infections in RAG KO Mice

Open Access
Diehl, Kevin
Area of Honors:
Immunology and Infectious Disease
Bachelor of Science
Document Type:
Thesis Supervisors:
  • Margherita Teresa-Anna Cantorna, Thesis Supervisor
  • Pamela Hankey Giblin, Honors Advisor
  • Vitamin D
  • Innate lymphoid cells
  • Citrobacter rodentium
  • Innate Immunity
  • IL-22
The goal of this study is to examine the role of vitamin D on the innate immune system. In order to eliminate any influences from the adaptive immune system, recombinase activated gene (RAG) knockout (KO) mice were used. This model makes it possible to study how vitamin D interacts with the innate immune system to modulate innate lymphoid cells (ILCs). ILC3s are crucial for early resistance to the enteric pathogen Citrobacter rodentium in mice. Groups of vitamin D sufficient (D+) and vitamin D deficient (D-) RAG KO mice were infected with C. rodentium. Mice were sacrificed, and the colons and small intestines were harvested for quantitative real-time PCR (qPCR) analysis. There was only a 50% infection rate, and the infection rate was not different between D+ and D- RAG KO mice. Given the low infection rate with the first experiment, the second cohort of mice was treated with vancomycin one day before infection to increase the rate of infection. D+ RAG KO mice had significantly higher expression of Il-22 compared to D- RAG KO mice. Vancomycin treatment increased the severity of infection in D- RAG KO mice. There was no effect of vitamin D on mRNA expression of Il-22, Reg3b, and Reg3g in the RAG KO mice pretreated with vancomycin. The data from this study may prove useful in increasing our understanding of how vitamin D modulates the activity of ILCs in terms of the innate immune system.