Recruitment of LC3 by Campylobacter jejuni to Bacterial Invasion Site on Host Cells via the Rac1-Mediated Signaling Pathway

<jats:p><jats:italic>Campylobacter jejuni</jats:italic> is a leading cause of food-borne disease worldwide. The pathogenicity of <jats:italic>C. jejuni</jats:italic> is closely associated with the internalization process in host epithelial cells, which is related to a host immune response. Autophagy indicates a key role in the innate immune system of the host to exclude invasive pathogens. Most bacteria are captured by autophagosomes and degraded by autophagosome-lysosome fusion in host cells. However, several pathogens, such as <jats:italic>Salmonella</jats:italic> and <jats:italic>Shigella</jats:italic>, avoid and/or escape autophagic degradation to establish infection. But autophagy involvement as a host immune response to <jats:italic>C. jejuni</jats:italic> infection has not been clarified. This study revealed autophagy association in <jats:italic>C. jejuni</jats:italic> infection. During infection, <jats:italic>C. jejuni</jats:italic> activated the Rho family small GTPase Rac1 signaling pathway, which modulates actin remodeling and promotes the internalization of this pathogen. In this study, we found the LC3 contribution to <jats:italic>C. jejuni</jats:italic> invasion signaling <jats:italic>via</jats:italic> the Rac1 signaling pathway. Interestingly, during <jats:italic>C. jejuni</jats:italic> invasion, LC3 was recruited to bacterial entry site depending on Rac1 GTPase activation just at the early step of the infection. <jats:italic>C. jejuni</jats:italic> infection induced LC3-II conversion, and autophagy induction facilitated <jats:italic>C. jejuni</jats:italic> internalization. Also, autophagy inhibition attenuated <jats:italic>C. jejuni</jats:italic> invasion step. Moreover, Rac1 recruited LC3 to the cellular membrane, activating the invasion of <jats:italic>C. jejuni</jats:italic>. Altogether, our findings provide insights into the new function of LC3 in bacterial invasion. We found the interaction between the Rho family small GTPase, Rac1, and autophagy-associated protein, LC3.</jats:p>