Heat-Killed Lacticaseibacillus paracasei ATG-E1 Improves Particulate Matter 10 Plus Diesel Exhaust Particles (PM10D)-Induced Airway Inflammation.

Air pollutants can cause respiratory diseases, highlighting the need for effective preventive and therapeutic strategies. We investigated the protective effects of heat-killed Lacticaseibacillus paracasei ATG-E1 against particulate matter plus diesel exhaust particle (PM10D)-induced airway inflammation. BALB/c mice were intranasally injected with PM10D and treated with heat-killed L. paracasei ATG-E1 via oral gavage for 5 days. In the bronchoalveolar lavage fluid (BALF) and lungs, inflammatory mediators, immune cell subtypes, and histological changes were analyzed, while gut microbiota composition was analyzed in the cecum. Heat-killed L. paracasei ATG-E1 suppressed the infiltration of immune cells, including neutrophils, T cells, and B cells. Furthermore, it decreased various inflammatory mediators, such as C-X-C Motif chemokine ligand (CXCL)-1, macrophage inflammatory protein (MIP)-2, interleukin (IL)-1α, and tumor necrosis factor (TNF)-α, in the BALF and lung tissue, as well as serum symmetric dimethylarginine (SDMA) levels in the PM10D-induced airway inflammation model. Heat-killed L. paracasei ATG-E1 also exhibited a protective effect against lung damage induced by PM10D. Furthermore, heat-killed L. paracasei ATG-E1 treatment shifted the gut microbiota composition, increasing several bacterial genera. The data demonstrate that heat-killed L. paracasei ATG-E1 acts as a protective agent against air pollutant-induced lung injury, suggesting its potential as a candidate adjunctive strategy for prevention.