[ODP-147] LC3 is utilized to the invasion of Campylobacter jejuni via Rac1 signaling pathway
Background: Campylobacter jejuni (Cj) is a leading cause of food-borne disease worldwide. The invasion process of Cj is an important process that triggers the virulence of this pathogen to host cells. Previously, we found association between autophagy signaling and Cj invasion. Here we suggested that autophagy facilitated Cj invasion, and found the association of autophagy to the classical Cj invasion signaling, especially actin polymerization factor, Rac1.
Method: Constitutive active (CA) form and dominant negative (DN) form of Rac1 GTPase was expressed in HeLa cell to investigate the association between autophagy signaling and Rac1 signaling in Cj invasion. Intracellular bacterial cell number was estimated by gentamycin protection assay.
Results & Discussion: Autophagy signaling was contributed to the invasion process in Cj. Additionally, we found the contribution of LC3 which well characterized as autophagosome protein to Cj invasion via the Rac1-mediated traditional invasion signaling pathway. Immunostaining of Cj infected cells revealed that LC3 was recruited to Cj in bacterial entry site, and this colocalization was frequently observed in CA-Rac expressed cell. Moreover, Campylobacter-fibronectin binding protein, CadF, activated Rac1 to recruit LC3 to the bacterial entry site. Our findings may provide means to the new function of autophagy in Cj infection.