Presentation Title

Itaconic Acid as the Antimicrobial Compound Delivered by the Rab32 Dependent Pathway to the Salmonella Containing Vacuole

Faculty Mentor

Dr. Theresa Rogers, Dr. Stefania Spano

Start Date

23-11-2019 8:00 AM

End Date

23-11-2019 8:45 AM

Location

67

Session

poster 1

Type of Presentation

Poster

Subject Area

biological_agricultural_sciences

Abstract

Typhoid fever is a dangerous diagnosis for many in developing countries, as poor sanitation and contaminated water sources provides the perfect environment for Salmonella enterica serovar Typhi to grow and infect a human host. In other animal models, the Rab32 dependent pathway can clear the infection by delivering an unknown antimicrobial compound to the Salmonella containing vacuole where S. Typhi grows in the macrophage. Another serovar, a related pathogen with a broader host range, Salmonella enterica serovar Typhimirium, has two effector proteins that can disrupt this pathway. Itaconic acid may be this antimicrobial compound, and the confirmation could lead to a deeper understanding of Salmonella and future treatments for typhoid fever. We infected wild type bone-marrow derived macrophages and macrophages with Irg1 knocked out with the wild type S. Typhimirium as well as S. Typhimirium with SopD2 and GtgE, two effector proteins that disrupt the Rab32 pathway, knocked out. Thus, we had four conditions to test to compare the growth between the wild type macrophages and the Irg1 knockout macrophages. The bacteria with the effector proteins knocked out were comparable to wild type S. Typhi. The This preliminary study shows that itaconic acid may not be the compound delivered, but these methods may be flawed as using the safer relative S. Typhimirium may result in degradation of the itaconic acid present in the wild type macrophages. Regardless, it is shown that the expression of Irg1, the gene ultimately responsible for itaconic acid production, has no effect on S. Typhimirium growth.

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Nov 23rd, 8:00 AM Nov 23rd, 8:45 AM

Itaconic Acid as the Antimicrobial Compound Delivered by the Rab32 Dependent Pathway to the Salmonella Containing Vacuole

67

Typhoid fever is a dangerous diagnosis for many in developing countries, as poor sanitation and contaminated water sources provides the perfect environment for Salmonella enterica serovar Typhi to grow and infect a human host. In other animal models, the Rab32 dependent pathway can clear the infection by delivering an unknown antimicrobial compound to the Salmonella containing vacuole where S. Typhi grows in the macrophage. Another serovar, a related pathogen with a broader host range, Salmonella enterica serovar Typhimirium, has two effector proteins that can disrupt this pathway. Itaconic acid may be this antimicrobial compound, and the confirmation could lead to a deeper understanding of Salmonella and future treatments for typhoid fever. We infected wild type bone-marrow derived macrophages and macrophages with Irg1 knocked out with the wild type S. Typhimirium as well as S. Typhimirium with SopD2 and GtgE, two effector proteins that disrupt the Rab32 pathway, knocked out. Thus, we had four conditions to test to compare the growth between the wild type macrophages and the Irg1 knockout macrophages. The bacteria with the effector proteins knocked out were comparable to wild type S. Typhi. The This preliminary study shows that itaconic acid may not be the compound delivered, but these methods may be flawed as using the safer relative S. Typhimirium may result in degradation of the itaconic acid present in the wild type macrophages. Regardless, it is shown that the expression of Irg1, the gene ultimately responsible for itaconic acid production, has no effect on S. Typhimirium growth.