Probiotic-derived exopolysaccharide interferes with TH2 priming and inhibits allergic inflammation
Year: 2023
Type: conference-abstract
Abstract: Allergic asthma is an increasing burden in industrialized countries, where treatments are limited to targeting symptoms and end-stage effectors rather than root causes. In recent years, the use of prophylactic, inhaled probiotic cocktails has shown promise in preventing allergic asthma. However, the mechanisms by which such probiotics prevent allergic symptoms and the exact bacterial product(s) responsible for probiotic activity remain to be elucidated. In this study, we focused on exopolysaccharide (EPS) from Bacillus subtilis, a ubiquitous soil bacterium that is commonly found as a dietary supplement. We found that in a mouse model of allergic airway disease, EPS treatment, prior to allergic sensitization and challenge, limits lung mucus hypersecretion and eosinophilia. Furthermore, EPS treatment inhibited accumulation of TH2, but not TH1 and TH17 subsets. To determine whether EPS was affecting TH2 cell priming by dendritic cells (DCs), we compared the composition and phenotype of DCs in the lung and mediastinal lymph nodes (medLN) after EPS treatment. Surprisingly, pre-treatment with EPS induced DC maturation as measured by an increase in costimulatory molecules and a decrease in the ability to uptake allergen and migrate to the medLN. DC maturation by EPS was TLR4-dependent, as TLR4 KO DCs did not respond to EPS. Together, our data suggest that EPS inhibits allergic sensitization by inducing DC maturation prior to allergen exposure, thereby leading to decreased TH2 priming and allergic inflammation. Thus, we provide a potential mechanism by which inhalation of a single probiotic-derived molecule can prevent the development of allergic inflammation. Supported by grants from NIH (3R01 AI125644-05S1, 1F31 HL156659-01A1)
Source: The Journal of Immunology
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W4385686672