Presenting Author: Tamara Vallejo-Schmidt
, Graduate Student at Towson Univ.
Abstract:
Uropathogenic Escherichia coli (UPEC), a pathogenic bacterium that causes urinary tract infections (UTIs), contains a virulence factor called TcpC. TcpC is a secreted toll/interleukin-1 receptor protein domain that aids UPEC evasion of the host immune system. TcpC has two known functions: (1) blocking mammalian toll-like receptor signaling pathways and (2) regulation of NAD+ glycohydrolase (NADase) activity in bacteria and host cells.Dictyostelium discoideum (D. discoideum), a soil dwelling amoeba, will be utilized. This model organism is vital due to conserved function and parallels to mammalian host-pathogen interactions. We hypothesize that TcpC and NADase activity blocks Discoideum signaling pathways. We will perform grazing resistance assays and qRT-PCR to (1) characterize interactions between TcpC-expressing bacteria and D. discoideum strains with gene deficiencies, and (2) compare phagocytosis gene expression in D. discoideum in the presence or absence of TcpC. Results show that D. discoideum grazes more efficiently on TcpC deficient E. coli strains. Preliminary data suggests that the NADase activity of TcpC may play a role in inhibition of Discoideum responses. Currently, we are exploring the effects of TcpC on D. discoideum signaling pathways to identify the mechanisms TcpC employs for inhibition. Understanding mechanisms Discoideum uses to phagocytize bacteria may allow for development of therapeutics for UTIs.
Analyzing TcpC-mediated modulation of D. discoideum signaling pathways in Uropathogenic Escherichia coli
Category
Poster
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Date: May 5 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1