Maintaining the intestinal epithelial barrier integrity is important for the defense against pathogen invasion and inflammation (Fasano and Shea-Donohue, 2005). In this regard, plasma DAO and D-lactate have been proposed as circulating markers for the extent of damage and repair of the intestinal mucosa (Wijtten et al., 2011; Zhao et al., 2014). These markers can reflect the intestinal permeability and barrier function in peripheral blood (Ewaschuk et al., 2005). Furthermore, TJs, such as claudin-1, occludin and ZO-1, have been proven to seal the lateral intercellular space and achieve an intact layer of epithelial cells that guard against pathogens (Groschwitz and Hogan, 2009; Suzuki, 2013). In the present study, the intermediate- and low-dose groups notably inhibited the increase in plasma DAO and D-lactate levels after ETEC infection. ETEC invasion has been reported to increase the release of DAO and D-lactate in the plasma and damage the intestinal epithelial cell membrane (Roselli et al., 2007; Yang et al., 2014; Xun et al., 2015). Hence, our results indicated that the strain exerts a protective effect on the host during ETEC invasion. Different doses of L. plantarum G83 prevented ETEC-induced membrane damage by inhibiting the delocalization of ZO-1 and consequently raising occludin and claudin-1 amounts. This effect is consistent with that observed by Roselli et al. (2007), who found higher occludin and ZO-1 mRNA expression in piglets fed with Lactobacillus sobrius than in those not fed with the strain. In the former piglets, ETEC-induced membrane damage was prevented by inhibiting the rearrangement of F-actin and dephosphorylation of occludin. As Mennigen and Bruewer (2009) reported, there is a close link between probiotics and regulation of intestinal permeability and barrier function. The above-mentioned findings collectively indicated that L. plantarum G83 exerts a protective effect against ETEC-induced membrane damage.