Teichoic Acids from Lactiplantibacillus plantarum AR113 Negatively Regulate Host Inflammatory Responses

The present study defines the negative impact of TAs from AR113 on the inflammatory response. Reducing TA production enhances the immunomodulatory effects of AR113 both in vitro and in vivo. Among the TAs, LTA and D-Ala exhibit distinct effects on the production of the anti-inflammatory cytokine IL-10, whereas WTA does not. In the context of colitis symptoms, LTA from AR113 contributes more significantly than WTA to inflammatory responses, particularly through the D-Ala branches in the LTA structure of AR113. Additionally, TAs produced by AR113 mediate colitis exclusively via immune-inflammatory pathways, and the intestinal barrier- protective effects of AR113 are independent of TAs.

本研究阐明了AR113来源的TAs（Teichoic Acids）对炎症应答的负面影响。降低TAs的合成水平可在体外与体内两种实验体系中增强AR113的免疫调节效应。在各类TAs中，脂磷壁酸（LTA，Lipoteichoic Acid）与D-丙氨酸（D-Ala，D-Alanine）可对抗炎细胞因子白细胞介素10（IL-10，Interleukin-10）的生成产生显著差异化调控作用，而壁磷壁酸（WTA，Wall Teichoic Acid）则无此类效果。针对结肠炎病症而言，AR113来源的LTA对炎症应答的促进作用显著强于WTA，该效应尤其依赖于AR113的LTA结构中的D-Ala侧链。此外，AR113产生的TAs仅通过免疫炎症通路介导结肠炎的发生，而AR113的肠屏障保护效应则不依赖于TAs。