the effect of lactobacillus actobacillus peptidoglycan on bovine β-lactoglobulin-sensitized mice via tlr2/nf-κb pathway

our previous study reported that lactobacillus acidophilus ( l.acidophilus )  key laboratory of dairy science  (klds) 1.0738 had an effective impact on inhibiting β-lactoglobulin (β-lg) allergy. this study further investigated the anti-allergic activity of peptidoglycan (pgn) isolated from klds 1.0738. this study aimed to assess whether toll-like receptor 2 (tlr2)/nf-kappab (nf-κb) signaling activated by pgn was responsible for reducing allergic inflammation. we first examined the role of pgn on cytokine production and tlr2 signaling expression of macrophages. then the immunoregulatory capacity of pgn was further evaluated by adopting the β-lg-sensitized mice model. the levels of sera ige, regulatory t cells (treg) and t-helper (th)17-related cytokine were detected by elisa. tlr2 signaling mrna and protein expression in colon tissues were measured by quantitative rt-pcr and western blot, respectively. our data showed that administration of  l. acidophilus pgn inhibited ige production and improved the treg/th17 balance toward a treg response in a mouse model of β-lg allergy. in addition, treating different doses l. acidophilus pgn to sensitized mice significantly increased tlr2 levels, along with enhancing nf-κb expression, especially in medium and high concentration ( p <0.05). further analysis revealed that the mrna expression of tlr2 and nf-κb were positively correlated with the foxp3 mrna expression ( p <0.05), but were negatively correlated with the rorγt mrna expression in l. acidophilus pgn-treated group compared to allergy group ( p <0.05). this study suggests pgn was similar to probiotics in preventing β-lg allergy through regulating treg/th17 imbalance, and activation of tlr2/nf-κb signaling may be involved in this process.