Exopolysaccharide from Lacticaseibacillus rhamnosus induces IgA production in airways and alleviates allergic airway inflammation in mouse model

The currently observed high prevalence of allergic diseases has been associated with changes in microbial exposure in industrialized countries. Defined bacterial components represent a new strategy for modulating the allergic immune response. We show that intranasal administration of exopolysaccharide (EPS) isolated from Lacticaseibacillus (L.) rhamnosus LOCK900 induces TGF-beta 1, IgA, and regulatory FoxP3(+) T-cells in the lungs of naive mice. Using the ovalbumin mouse model, we demonstrate that intranasal administration of EPS downregulates the development of allergic airway inflammation and the Th2 cytokine response in sensitized individuals. At the same time, EPS treatment of sensitized mice, similar to EPS-induced responses in naive mice, significantly increased the level of total, OVA-specific, and also bacteria-specific IgA in bronchoalveolar lavage and the number of IgA-producing B-cells in the lung tissue of these mice. Thus, EPS derived from L. rhamnosus LOCK900 can be considered a safe candidate for preventing the development of allergic symptoms in the lungs of sensitized individuals upon exposure to an allergen.

Automated summary

The high prevalence of allergic diseases in industrialized countries is believed to be related to changes in microbial exposure. The administration of exopolysaccharide (EPS) from Lacticaseibacillus (L.) rhamnosus LOCK900 induces immune responses in the lungs of mice, leading to a reduction in allergic airway inflammation and Th2 cytokine response in sensitized individuals. Furthermore, EPS treatment increases the production of IgA in the lungs of sensitized mice. These findings suggest that EPS derived from L. rhamnosus LOCK900 could be a safe candidate for preventing the development of allergic symptoms in sensitized individuals.