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. 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.
Keywords: Peptidoglycan; Regulatory; T-lymphocytes; TLR2/NF-κB signaling; Th17 cells; β-lactoglobulin allergy.