L.acidophilus participates in intestinal inflammation induced by PM2.5 through affecting the Treg/Th17 balance

Particulate matter with aerodynamic diameters of ≤2.5 μm (PM2.5) is associated with multiple organ damage, among which the influence of PM2.5 on the gastrointestinal system has been a recent focus of attention. In this study, four different types of PM2.5 exposure models are established to determine the occurrence of PM2.5 induced intestinal inflammation. In view of the abnormal expression of lymphocytes detected in the model and the well-known fact that the intestine is the largest immune organ, we focused on the intestinal immune system. A combined regulatory T cell (Treg) transplantation experiment demonstrated that PM2.5 induced intestinal inflammation by affecting the imbalance of regulatory T cell/T helper cell 17 (Treg/Th17). Since the intestine has the highest microbial content, and the results of the 16S rDNA third-generation sequencing analysis further revealed that the abundance of Lactobacillus_acidophilus (L.acidophilus) decreased significantly after PM2.5 exposure. The following mechanism study confirmed that L.acidophilus participated in an imbalance of Treg/Th17. Moreover, L.acidophilus supplementation successfully alleviated intestinal inflammation by regulated regulating the balance of Treg/Th17 under the background of PM2.5 exposure. Hence, this is a potential method to protect against intestinal inflammation induced by PM2.5.