NOD1 and its role in the survival of S. typhimurium inside the host cell.

RODOLFO M. ORTIZ FLORES; FRANCISCO GARCÍA DEL PORTILLO; WALTER BERÓN

Buenos Aires

Congreso; Reunión Conjunta de Sociedades de Biociencias: LIII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB).; 2017

Reunión Conjunta de Sociedades de Biociencias: LIII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB).

NOD1, a member of NOD-like receptor protein family and is a close relative of NOD2, is an intracellular pattern recognition receptor involved in recognizing bacterial peptidoglycan fragments that localize to the cytosol. NOD1 activation triggers inflammation, antimicrobial mechanisms and autophagy in both epithelial cells. FYCO1 (FYVE and coiled-coil protein 1) is a transport adaptor that binds to LC3 to mediate transport of late endosomes and autophagosomes along microtubules in the plus end direction. S. enterica serovar Typhimurium (S. Typhimurium) is an intracellular bacterial pathogen that infects phagocytic and nonphagocytic eukaryotic cells and resides in a specialized phagosomal compartment named the SCV. In previous work, the role of autophagy during Salmonella survival within the cell has been demonstrated. To determine the role of NOD1 in relationship with FYCO1 and LC3 in the survival of Salmonella, NRK-49F cells were transfected with pEGFP or pEGFP-NOD1, pEGFP-LC3, pEGFP-FYCO1 and the negative mutants and then infected with Salmonella. For Indirect Immunofluorescence cells were processed and following parameters were determined: number of infected cells, Salmonella intracellular multiplication and Salmonella intracellular distribution. The results showed that wild type or mutants forms of overexpressed proteins significantly affecting these parameters. In conclusion, the results presented here try to approximate a mechanism for the survival of Salmonella during its interaction with the autophagy process of the host cell.