Fig. 6
Proposed model for GABABR activation accelerating autophagy formation by inhibiting MyD88 signaling to strengthen EGC antibacterial activity. Pretreatment of EGCs with the GABABR agonist baclofen significantly decreased MyD88 levels upon infection with ETECK88. Over time, the number of autophagosomes and lysosomes increased, and the number of autolysosomes increased, suggesting that autophagy intensified. Importantly, the number of autolysosomes and the extent of their colocalization with ETECK88 were obviously elevated in the infected cells. Furthermore, the levels of the proinflammatory factors IL-1β and IL-6 decreased, while the production of the anti-inflammatory mediator TGF-β increased. Hence, the antibacterial function of EGCs was ultimately reinforced